Hubbry Logo
Urinary systemUrinary systemMain
Open search
Urinary system
Community hub
Urinary system
logo
8 pages, 0 posts
0 subscribers
Be the first to start a discussion here.
Be the first to start a discussion here.
Urinary system
Urinary system
Urinary system
View on Wikipedia
from Wikipedia

Urinary system
1. Human urinary system: 2. Kidney, 3. Renal pelvis, 4. Ureter, 5. Urinary bladder, 6. Urethra. (Left side with frontal section)
7. Adrenal gland
Vessels: 8. Renal artery and vein, 9. Inferior vena cava, 10. Abdominal aorta, 11. Common iliac artery and vein
Translucent: 12. Liver, 13. Large intestine, 14. Pelvis
Urinary system in the male. Urine flows from the kidneys via the ureters into the bladder where it is stored until it exits the body through the urethra (longer in males, shorter in females) during urination
Details
Identifiers
Latinsystema urinarium
MeSHD014551
TA98A08.0.00.000
TA23357
FMA7159
Anatomical terminology

The urinary system, also known as the urinary tract or renal system, is a part of the excretory system of vertebrates. In humans and placental mammals, it consists of the kidneys, ureters, bladder, and the urethra. The purpose of the urinary system is to eliminate urine from the body, regulate blood volume and blood pressure, control levels of electrolytes and metabolites, and regulate blood pH.[1] The kidneys have an extensive blood supply via the renal arteries which leave the kidneys via the renal vein. Each kidney consists of functional units called nephrons. Following filtration of blood and further processing, the ureters carry urine from the kidneys into the urinary bladder. The urethra carries urine from the bladder through the penis or vulva during urination. The female and male urinary system are very similar, differing only in the length of the urethra.[2]

800–2,000 milliliters (mL) of urine are normally produced every day in a healthy human. This amount varies according to fluid intake and kidney function.

Structure

[edit]
3D model of urinary system

The urinary system refers to the structures that produce and excrete urine. In the human urinary system there are two kidneys that are located between the dorsal body wall and parietal peritoneum on both the left and right sides.

The formation of urine begins within the functional unit of the kidney, the nephrons. Urine then flows through the nephrons, through a system of converging tubules called collecting ducts. These collecting ducts then join to form the minor calyces, followed by the major calyces that ultimately join the renal pelvis. Urine flows from the renal pelvis into the ureter, which transports urine into the urinary bladder. The anatomy of the human urinary bladder and urethra differs between males and females. In males, the urethra begins at the internal urethral orifice in the trigone of the bladder, and then becomes the prostatic, membranous, bulbar, and penile urethra. Urine exits the male urethra through the urinary meatus in the glans penis. The female urethra is much shorter, beginning at the bladder neck and terminating in the vulval vestibule.

Development

[edit]
Main article: Development of the urinary system

Microanatomy

[edit]
See also: Urothelium

Under microscopy, the urinary system is covered in a unique lining called urothelium, a type of transitional epithelium. Unlike the epithelial lining of most organs, transitional epithelium can flatten and distend. Urothelium covers most of the urinary system, including the renal pelvis, ureters, and bladder.

Function

[edit]

The main functions of the urinary system and its components are to:

Urine formation

[edit]

Average urine production in adult humans is about 1–2 litres (L) per day, depending on state of hydration, activity level, environmental factors, weight, and the individual's health. Producing too much or too little urine requires medical attention. Polyuria is a condition of excessive urine production (> 2.5 L/day). Conditions involving low output of urine are oliguria (< 400 mL/day) and anuria (< 100 mL/day).

The first step in urine formation is the filtration of blood in the kidneys. In a healthy human, the kidney receives between 12 and 30% of cardiac output, but it averages about 20% or about 1.25 L/min.

The basic structural and functional unit of the kidney is the nephron. Its chief function is to regulate the concentration of water and soluble substances like sodium by filtering the blood, reabsorbing what is needed and excreting the rest as urine.

In the first part of the nephron, Bowman's capsule filters blood from the circulatory system into the tubules. Hydrostatic and osmotic pressure gradients facilitate filtration across a semipermeable membrane. The filtrate includes water, small molecules, and ions that easily pass through the filtration membrane. However, larger molecules such as proteins and blood cells are prevented from passing through the filtration membrane. The amount of filtrate produced every minute is called the glomerular filtration rate or GFR and amounts to 180 litres per day. About 99% of this filtrate is reabsorbed as it passes through the nephron and the remaining 1% becomes urine.

The urinary system is regulated by the endocrine system by hormones such as antidiuretic hormone, aldosterone, and parathyroid hormone.[3]

Regulation of concentration and volume

[edit]

The urinary system is under influence of the circulatory system, nervous system, and endocrine system.

Aldosterone plays a central role in regulating blood pressure through its effects on the kidney. It acts on the distal tubules and collecting ducts of the nephron and increases reabsorption of sodium from the glomerular filtrate. Reabsorption of sodium results in retention of water, which increases blood pressure and blood volume. Antidiuretic hormone (ADH), is a neurohypophysial hormone found in most mammals. Its two primary functions are to retain water in the body and vasoconstriction. Vasopressin regulates the body's retention of water by increasing water reabsorption in the collecting ducts of the kidney nephron.[4] Vasopressin increases water permeability of the kidney's collecting duct and distal convoluted tubule by inducing translocation of aquaporin-CD water channels in the kidney nephron collecting duct plasma membrane.[5]

Urination

[edit]
Main article: Urination

Urination, also sometimes referred to as micturition, is the ejection of urine from the urinary bladder to the outside of the body. Urine is ejected through the urethra from the penis or vulva in placental mammals and through the cloaca in other vertebrates. In healthy humans (and many other animals), the process of urination is under voluntary control. In infants, some elderly individuals, and those with neurological injury, urination may occur as an involuntary reflex. Physiologically, micturition involves coordination between the central, autonomic, and somatic nervous systems. Brain centers that regulate urination include the pontine micturition center, periaqueductal gray, and the cerebral cortex.

Clinical significance

[edit]
Main article: Urologic disease
Further information: Urinary tract infection

Urologic disease can involve congenital or acquired dysfunction of the urinary system. As an example, urinary tract obstruction is a urologic disease that can cause urinary retention.

Diseases of the kidney tissue are normally treated by nephrologists, while diseases of the urinary tract are treated by urologists. Gynecologists may also treat female urinary incontinence.

Diseases of other bodily systems also have a direct effect on urogenital function. For instance, it has been shown that protein released by the kidneys in diabetes mellitus sensitizes the kidney to the damaging effects of hypertension.[6]

Diabetes also can have a direct effect in urination due to peripheral neuropathies, which occur in some individuals with poorly controlled blood sugar levels.[7]

Urinary incontinence can result from a weakening of the pelvic floor muscles caused by factors such as pregnancy, childbirth, aging, and being overweight. Findings recent systematic reviews demonstrate that behavioral therapy generally results in improved urinary incontinence outcomes, especially for stress and urge UI, than medications alone.[8][9] Pelvic floor exercises known as Kegel exercises can help in this condition by strengthening the pelvic floor. There can also be underlying medical reasons for urinary incontinence which are often treatable. In children, the condition is called enuresis.

Some cancers also target the urinary system, including bladder cancer, kidney cancer, ureteral cancer, and urethral cancer. Due to the role and location of these organs, treatment is often complicated.[citation needed]

History

[edit]

Kidney stones have been identified and recorded about as long as written historical records exist.[10] The urinary tract including the ureters, as well as their function to drain urine from the kidneys, has been described by Galen in the second century AD.[11]

The first to examine the ureter through an internal approach, called ureteroscopy, rather than surgery was Hampton Young in 1929.[10] This was improved on by VF Marshall who is the first published use of a flexible endoscope based on fiber optics, which occurred in 1964.[10] The insertion of a drainage tube into the renal pelvis, bypassing the ureters and urinary tract, called nephrostomy, was first described in 1941. Such an approach differed greatly from the open surgical approaches within the urinary system employed during the preceding two millennia.[10]

See also

[edit]

References

[edit]
[edit]
Revisions and contributorsEdit on WikipediaRead on Wikipedia

Urinary system

View on Grokipedia
from Grokipedia
The urinary system, also known as the renal system, is the responsible for producing, storing, and eliminating to maintain fluid, , and acid-base balance in the body. It consists of two kidneys, two ureters, the urinary , and the , working together to filter blood and remove metabolic wastes such as and excess ions. In humans, the kidneys filter approximately 200 liters of fluid daily from the bloodstream, reabsorbing essential substances while forming about 1 to 2 liters of for . The kidneys, bean-shaped organs located retroperitoneally on either side of the spine between the 12th thoracic and 3rd , serve as the core of the system. Each kidney contains about 1 million nephrons, the microscopic functional units that perform , , and to regulate blood composition. Beyond waste removal, the kidneys produce hormones including for formation, renin for blood pressure control, and the active form of for calcium . Urine formed in the kidneys flows through the ureters—muscular tubes about 25 to 30 centimeters long—into the via peristaltic contractions. The , a muscular sac in the , stores up to 400 to 600 milliliters of until voluntary expulsion through the during micturition, a process coordinated by the . Disruptions in this system can lead to conditions like urinary tract infections or , underscoring its vital role in .

Anatomy

Gross anatomy

The urinary system consists of the paired kidneys, ureters, urinary bladder, and urethra, which collectively form a continuous tract for urine transport and storage. The kidneys are bean-shaped, retroperitoneal organs located on either side of the vertebral column, extending from the T12 to L3 vertebral levels, with the right kidney positioned slightly inferior to the left due to the liver's influence. Each kidney measures approximately 11-14 cm in length, 6 cm in width, and 4 cm in thickness, weighing about 150 g in adults, and features a medial concavity at the hilum where structures enter and exit. The ureters are muscular tubes, each about 25 cm long and 3-4 mm in diameter, that extend from the to the , coursing retroperitoneally along the posterior before entering the . They descend anterior to the , cross the common iliac arteries at the , and insert obliquely into the wall to prevent . The is a hollow, muscular organ situated in the behind the , with a capacity of 400-600 mL in adults; its wall consists of arranged in a pattern for contraction during voiding. The urethra conveys urine from the bladder to the exterior, differing significantly between sexes due to its role in reproduction in males. In females, it is short (3-4 cm) and embedded in the anterior vaginal wall, opening anterior to the vaginal orifice. In males, it measures about 20 cm and is divided into prostatic (passing through the prostate), membranous (traversing the pelvic floor), and spongy (or penile) portions extending through the penis. Supporting structures include the fibrous renal capsule enveloping each kidney, a perirenal fat layer cushioning and anchoring it, and the adrenal glands situated superiorly on each kidney's medial border. Vascular supply arises from the renal arteries branching directly from the abdominal aorta at the L1-L2 level, entering the hilum and dividing into segmental branches, while renal veins drain into the inferior vena cava.

Microscopic anatomy

The microscopic anatomy of the urinary system is characterized by specialized cellular and tissue structures that facilitate urine formation and transport, with the serving as the primary functional unit in the . The consists of a and a renal tubule, embedded within the and medulla, supported by interstitial . Key cellular components include epithelial cells adapted for selective permeability and , as well as supportive vascular and muscular elements. The , located in the , comprises the —a tuft of fenestrated capillaries—and , a double-layered epithelial structure that encloses it. The visceral layer of is formed by podocytes, highly specialized cells with interdigitating foot processes that create filtration slits approximately 25–30 nm wide, bridged by slit diaphragms to regulate plasma filtration. The parietal layer consists of , continuous with the at the urinary pole. The renal tubule begins with the proximal convoluted tubule (PCT) in the cortex, lined by featuring a prominent brush border of microvilli on the apical surface to enhance reabsorptive surface area. This transitions into the , which dips into the medulla; the descending thin limb is lined by for passive , while the ascending limb includes a thick segment with simple cuboidal cells lacking a . The (DCT), also in the cortex, features with fewer organelles, a more prominent lumen, and no microvilli, distinguishing it from the PCT. Multiple DCTs converge into collecting ducts, lined by simple cuboidal to low columnar epithelium containing principal cells that express channels in their apical membranes for water permeability. At the vascular pole of the , the integrates tubular and vascular elements for local regulation. It includes the , a plaque of tall, closely packed columnar cells in the DCT wall that sense tubular fluid composition via densely stained nuclei and basal Golgi apparatus. Adjacent , modified cells in the afferent wall, contain secretory granules with renin. Extraglomerular provide structural support between these components. Beyond the nephron, the ureters, , and feature protective epithelia and contractile tissues. The ureters are lined by (urothelium), a stratified structure with dome-shaped superficial umbrella cells that allow distension without damage, overlying a and layers of (inner longitudinal, middle circular, outer longitudinal). The wall includes the same , supported by a thick and the , an interwoven mass of fibers arranged in inner and outer longitudinal and middle circular layers for forceful contraction. The proximal retains , transitioning distally to stratified squamous. Ureteral facilitates peristaltic urine propulsion through helical and longitudinal orientations. The renal provides structural framework and includes the cortical , medullary rays, and pyramids. The cortical consists of renal corpuscles and convoluted tubules embedded in stroma with fibroblasts and . Renal columns are extensions of cortical tissue projecting into the medulla, separating adjacent medullary structures. The medullary pyramids, 8–18 conical structures per kidney, contain parallel arrays of collecting ducts, vasa recta, and thin loops of Henle within a denser rich in fibroblasts and glycosaminoglycans. Medullary rays, extensions of the pyramids into the cortex, house straight tubules and collecting ducts.

Embryological development

The development of the urinary system begins in the fourth week of embryonic life with the formation of the nephrogenic cord from , along which three successive kidney structures emerge in a rostral-to-caudal sequence. The pronephros, the most primitive and transient stage, forms around week 4 but rapidly degenerates without contributing significantly to the permanent urinary system in humans. This is followed by the mesonephros, which develops from weeks 5 to 7 (peaking around week 6), functions temporarily in urine production, and partially regresses; its duct (Wolffian duct) persists and contributes to the male reproductive ducts. The metanephros, arising from week 5 onward, becomes the definitive through interactions between the ureteric bud and metanephric mesenchyme. The key inductive process for metanephric development involves the outgrowth of the ureteric bud from the caudal around week 5, which invades the adjacent metanephric derived from the nephrogenic cord. This reciprocal induction—where the ureteric bud signals the mesenchyme via factors like GDNF and the mesenchyme responds with branching —leads to the formation of the from the bud's branches and nephron precursors from the mesenchyme. Nephron segmentation occurs through mesenchymal-to-epithelial transition, sequentially forming the , , , and distal tubule, which connect to the collecting ducts; this process ensures the mature structure. The lower urinary tract originates from the , an endodermal structure that divides around week 7 by the urorectal septum into the anterior and posterior anorectal canal. The 's cranial portion expands to form the , incorporating contributions from the at its apex (which regresses to the ), while the caudal portion develops into the prostatic and in males or the entire in females. The ureters insert into the via separate orifices, establishing the ureterovesical junction critical for antireflux mechanisms. Disruptions in these processes can lead to congenital anomalies. Renal agenesis results from failure of the metanephric to induce or respond to the ureteric bud, leading to unilateral or bilateral absence of kidney tissue. arises from abnormal fusion of the metanephroi at their lower poles during the kidney's cranial ascent from the to the between weeks 6 and 9, preventing independent rotation and fixation. stems from defective formation of the ureterovesical junction, often due to short intramural segments or abnormal ureteral orifice positioning during incorporation. Nephron formation continues throughout gestation, with all s generated by weeks 32 to 36, after which the kidneys produce to contribute to volume from week 10 onward; however, full functional maturity, including complete nephron maturation and vascularization, occurs postnatally.

Physiology

Glomerular filtration

Glomerular filtration is the initial passive process in formation, occurring within the glomeruli of the nephrons, where is filtered to produce an ultrafiltrate that enters . This filtration relies on the across the glomerular capillaries and the selective permeability of the filtration barrier, allowing the passage of and small solutes while retaining larger components. The process is driven by the heart's pumping action, which generates hydrostatic pressure in the glomerular capillaries, and it occurs continuously at a rate that maintains fluid and solute . The glomerular filtration barrier consists of three layered structures that provide both size and charge selectivity. The innermost layer features fenestrated endothelial cells of the glomerular capillaries, with pores approximately 70-100 nm in diameter that permit the free passage of , ions, and molecules up to about 70 while restricting larger elements like cells. The middle layer, the (GBM), is a gel-like matrix composed primarily of , IV, and nidogen, which is negatively charged due to proteoglycans such as ; this charge repels anionic proteins like (molecular weight ~66 ) and further sieves molecules based on size, effectively excluding those larger than 4-5 nm in hydrodynamic radius. The outermost layer comprises foot processes, which interdigitate to form slits of 4-11 nm width bridged by a slit diaphragm (primarily nephrin and podocin proteins), acting as the final barrier to prevent passage of proteins exceeding ~70 and ensuring minimal protein loss into the filtrate. Damage to any layer, such as effacement, can compromise this barrier and lead to . The (GFR) quantifies the volume of fluid filtered per unit time, typically averaging 125 mL/min in healthy adults (or ~180 L/day), representing about 20% of the renal plasma flow. GFR is determined by the Starling forces across the capillary wall, governed by the equation: GFR=Kf×[(PGC−PBS)−(πGC−πBS)]\text{GFR} = K_f \times [(P_{GC} - P_{BS}) - (\pi_{GC} - \pi_{BS})] where KfK_f is the filtration coefficient (reflecting membrane permeability and surface area, approximately 12.5 mL/min/mmHg), PGCP_{GC} is glomerular capillary hydrostatic (~55 mmHg, favoring ), PBSP_{BS} is Bowman's hydrostatic (~15 mmHg, opposing ), πGC\pi_{GC} is glomerular capillary oncotic (~30 mmHg, opposing due to plasma proteins), and πBS\pi_{BS} is Bowman's oncotic (~0 mmHg). This yields a net filtration of 10-15 mmHg along the capillary length, sufficient to drive despite the low . The filtration coefficient KfK_f can vary with pathological changes in membrane area or permeability. The resulting glomerular filtrate is an ultrafiltrate of plasma, containing , electrolytes (e.g., sodium, potassium, chloride, ), glucose, , and small metabolites like and , but virtually free of proteins larger than 70 kDa and cellular elements. Its composition mirrors plasma in terms of small solutes (concentrations nearly identical for freely filterable substances), with a protein content less than 0.03 g/dL compared to plasma's 7 g/dL, ensuring that over 99% of filtered and solutes are available for subsequent tubular processing. This selective filtration sets the stage for the nephron's role in waste excretion and . Regulation of GFR occurs primarily through intrinsic autoregulatory mechanisms to maintain stability despite fluctuations in systemic (typically between 80-180 mmHg ). The myogenic response involves intrinsic contraction of vascular in the afferent in response to increased wall tension from rising pressure, thereby reducing blood flow into the and stabilizing PGCP_{GC}. , mediated by the , senses elevated NaCl delivery to the in the distal tubule (due to high GFR), triggering release that constricts the afferent to lower GFR. These mechanisms collectively buffer changes in filtration, preventing overload or underperfusion of the .

Tubular reabsorption and secretion

Tubular reabsorption and secretion are essential processes in the that modify the glomerular filtrate, reclaiming vital substances and eliminating wastes to maintain . The kidneys filter approximately 180 liters of plasma daily, producing an ultrafiltrate that is nearly identical to plasma in composition, but tubular mechanisms reabsorb about 99% of this volume, primarily through driven by ATP-consuming pumps like the Na⁺/K⁺-ATPase on the basolateral membrane of tubular cells. This enzyme creates a sodium gradient that powers secondary active transport of solutes across the apical membrane, with water following osmotically. Secretion, conversely, adds substances from into the tubular lumen, enhancing clearance of certain metabolites. In the proximal tubule, which handles the bulk of reabsorption, approximately 65% of filtered sodium, water, chloride, bicarbonate, glucose, and amino acids are reclaimed. Sodium entry occurs via apical cotransporters such as the sodium-glucose linked transporter 2 (SGLT2) for glucose (responsible for 80-90% of filtered glucose reabsorption) and sodium-amino acid cotransporters, while bicarbonate is reabsorbed through carbonic anhydrase-mediated processes involving Na⁺/H⁺ exchange. Water and chloride follow paracellularly due to the osmotic gradient and solvent drag, respectively, ensuring isosmotic reabsorption without significant dilution or concentration of the tubular fluid. The contributes to solute recovery through its countercurrent multiplier configuration, where the descending limb is permeable to water and the ascending limb actively transports ions. In the thick ascending limb, 15-25% of filtered NaCl is reabsorbed via the apical Na⁺-K⁺-2Cl⁻ cotransporter (NKCC2), powered by the basolateral Na⁺/K⁺-ATPase, creating a dilute tubular and establishing the medullary osmotic gradient essential for further processing. Fine-tuning occurs in the distal convoluted tubule and collecting duct, where and adjust levels based on physiological needs. Sodium here, about 5-10% of the filtered load, is mediated by the (ENaC) in principal cells of the collecting duct, stimulated by aldosterone to promote via apical ROMK channels. Calcium reabsorption in the distal tubule is regulated by (PTH), which activates basolateral calcium-sensing receptors and enhances apical TRPV5 channels for . increases along the distal nephron, driven by the from sodium . Tubular secretion primarily involves organic anions and cations, handled by specific transporters in the to clear drugs, toxins, and metabolic byproducts. For instance, para-aminohippurate (PAH) is secreted via organic anion transporters (OAT1 and OAT3) on the basolateral membrane and MRP2/4 on the apical side, achieving near-complete extraction in one pass and serving as a marker for effective renal plasma . This process complements by augmenting the clearance of protein-bound solutes that do not freely filter at the .

Urine concentration and dilution

The kidneys adjust urine osmolarity and volume through specialized mechanisms in the loop of Henle and collecting ducts, enabling the production of that ranges from highly concentrated to dilute as needed for or . This process relies on the establishment of an osmotic gradient in the , where interstitial osmolarity increases progressively from the cortex (approximately 300 mOsm/L) to the inner medulla (up to 1200 mOsm/L in humans), facilitating reabsorption without energy expenditure beyond solute . The countercurrent multiplier system in the loop of Henle generates this medullary hyperosmolarity. In juxtamedullary nephrons, the descending limb is permeable to but relatively impermeable to solutes, allowing equilibration with the increasingly hyperosmotic as filtrate descends. The ascending limb, impermeable to , actively transports NaCl out via the Na-K-2Cl cotransporter, diluting the tubular fluid while adding solutes to the ; this single-effect difference (about 200 mOsm/L per level) is multiplied longitudinally along the loop due to countercurrent flow, culminating in medullary osmolarities of up to 1200 mOsm/L. The vasa recta function as a countercurrent exchanger, with descending vessels gaining solutes and from the hyperosmotic and ascending vessels returning them, thereby preserving the by minimizing solute washout despite medullary blood flow. Antidiuretic hormone (ADH, or ) regulates final urine concentration by modulating water permeability in the collecting ducts. In response to plasma hyperosmolarity or , ADH binds to V2 receptors on principal cells, activating a cAMP-mediated pathway that translocates (AQP2) water channels from intracellular vesicles to the apical membrane. This insertion allows osmotic water reabsorption into the hyperosmotic medulla, concentrating urine to match interstitial osmolarity (up to ~1200 mOsm/L) and minimizing water loss; without ADH, AQP2 remains internalized, rendering the ducts impermeable to water. Urine dilution occurs primarily in the absence of ADH, leveraging the ascending limb's impermeability to and active NaCl , which reduces tubular fluid osmolarity to as low as ~100 mOsm/L by the early distal tubule—hypoosmotic relative to plasma. As this dilute fluid reaches the ducts without ADH-induced water permeability, it remains hypoosmotic, enabling of excess during overhydration; maximal dilution can produce at ~50 mOsm/L under conditions of high fluid intake. Urea recycling enhances the medullary gradient, particularly in the inner medulla. Urea is freely filtered and partially reabsorbed in the and inner medullary collecting ducts (facilitated by urea transporters UT-A1/3 under ADH influence), then diffuses into the ; some re-enters the thin ascending limb or descending vasa recta, recycling back to maintain high interstitial concentrations (up to 50% of total osmolarity in the papilla). This process amplifies the osmotic gradient without additional NaCl transport, supporting maximal concentration. In healthy adults, these mechanisms yield a daily urine output of approximately 1-2 liters, varying with fluid and ADH levels to maintain balance; for instance, with normal of about 2 liters, output stabilizes around 1.5 liters after reabsorbing 99% of filtered .

Micturition

Micturition, or , is the process by which the urinary empties its contents through coordinated neural and muscular mechanisms. During the storage phase, the fills gradually with urine produced by the kidneys, and stretch receptors embedded in the wall detect increasing distension as volume rises. These receptors, primarily Aδ and C-fiber afferents, transmit sensory signals via pelvic nerves to the sacral , providing feedback on fullness. The exhibits remarkable accommodation, maintaining low intravesical pressure despite filling to a capacity of approximately 400–600 mL in healthy adults, allowing for comfortable storage without frequent urges. This accommodation is facilitated by the viscoelastic properties of the bladder wall and inhibitory neural inputs that promote relaxation during filling. The first sensation of urge typically occurs at around 200–300 mL, signaling the transition toward the voiding phase, though voluntary control can defer micturition until a more critical threshold is reached. The micturition reflex arc is orchestrated by a hierarchical neural system involving spinal and supraspinal centers. At the spinal level, afferent signals from stretch receptors synapse in the sacral parasympathetic nucleus (S2–S4), which coordinates detrusor contraction via preganglionic neurons in the pelvic . Sympathetic innervation from the thoracolumbar (T10–L2), via hypogastric , provides tonic inhibition of the detrusor during storage by activating β-adrenergic receptors, while also facilitating internal contraction through α-adrenergic pathways. Higher coordination occurs in the pontine micturition center (PMC) in the , which integrates inputs from the and to synchronize detrusor contraction with relaxation, ensuring efficient voiding. Two regulate urine flow: the , composed of at the neck, operates involuntarily under sympathetic control to remain closed during storage and relaxes during voiding via inhibition of α-adrenergic tone. The external urethral sphincter, made of striated muscle innervated by somatic pudendal nerves (S2–S4), allows voluntary control, contracting to maintain continence and relaxing on command to initiate . The voiding process begins with voluntary relaxation of the external sphincter and PMC-mediated inhibition of sympathetic outflow, leading to internal sphincter opening and detrusor contraction that generates intravesical pressure exceeding urethral resistance. This coordinated action propels through the , typically completing in seconds to minutes, with the reflex sustained until the empties sufficiently to deactivate input. In pediatric development, micturition is initially reflexive and involuntary in infants, driven by spinal mechanisms without cortical inhibition, resulting in spontaneous voiding. Voluntary control emerges around 2–3 years of age through potty training, as myelination of descending pathways from the matures, enabling integration of sensory cues with behavioral restraint until age 3–5 years. In the elderly, age-related changes such as reduced detrusor contractility, afferent degeneration, and weakened muscles increase risks of incomplete emptying and urgency incontinence, though baseline physiology remains similar to younger adults absent pathology.

Homeostatic roles

Fluid and electrolyte balance

The urinary system plays a central role in maintaining and balance by regulating the and of water and ions, ensuring osmotic stability and cellular function across the body. Through the kidneys' and tubular processes, approximately 180 liters of glomerular filtrate are produced daily, with over 99% reabsorbed to adjust for intake and losses, preventing imbalances that could lead to , , or cellular dysfunction. This integrates neural, hormonal, and renal mechanisms to respond to changes in and volume. Water balance is achieved by balancing daily intake, primarily from beverages and food (about 2-3 liters), against losses via insensible routes like and lungs (0.5-1 liter) and (1-2 liters under normal conditions). The kidneys conserve water during deficits by reducing output to as low as 0.5 liters per day, primarily through the action of antidiuretic hormone (ADH), which enhances water permeability in the collecting ducts. Hypothalamic osmoreceptors detect increases in above 280-285 mOsm/kg, triggering ADH release from the to restore balance. Thirst mechanisms complement renal conservation, as osmoreceptors in the stimulate drinking when osmolality rises, typically increasing fluid intake to dilute plasma and lower osmolality back to 280-295 mOsm/kg. This osmoregulatory axis ensures that even small deviations in (1-2% loss) prompt corrective responses, maintaining total at about 60% of body weight in adults. Disruptions, such as excessive intake without ADH response, can lead to , while deficits cause . Sodium, the primary extracellular fluid (ECF) cation, is regulated to maintain ECF volume and osmolality, with daily intake of 3-6 grams balanced by renal excretion. The kidneys reabsorb over 99% of filtered sodium (about 25,000 mmol/day), primarily in the proximal tubule and loop of Henle, but fine-tune it in the distal nephron under aldosterone influence. Aldosterone, released from the adrenal cortex in response to low ECF volume or hyperkalemia, binds to mineralocorticoid receptors in principal cells, upregulating epithelial sodium channels (ENaC) and Na+/K+-ATPase to enhance reabsorption, thereby preventing natriuresis during volume depletion. Potassium relies on renal to counter dietary (50-100 mmol/day), as the kidneys excrete 90-95% of ingested , mainly in the distal . In the cortical collecting duct, principal cells secrete via channels, driven by the established by Na+ reabsorption and aldosterone stimulation, which increases Na+/+- activity. This process adjusts to plasma levels, with (>5.5 mmol/L) enhancing to avoid cardiac arrhythmias, while (<3.5 mmol/L) reduces it, though chronic low risks . Flow rate in the distal tubule also modulates , with higher flows increasing K+ delivery and excretion. Chloride, the major ECF anion, follows sodium passively through paracellular pathways in the and thick ascending limb, maintaining electroneutrality without specific . Calcium, another key divalent cation, is filtered at approximately 10 g/day and 98-99%, primarily in the (65%), (25%), and distal tubule (8%), regulated by (PTH) which inhibits to lower serum levels, and by the active form of which promotes it for mineralization and neuromuscular function; normal serum calcium is 2.2-2.6 mmol/L (8.8-10.4 mg/dL). For magnesium and , the kidneys filter approximately 4 g of magnesium and 6 g of daily, 95-99% to prevent hypomagnesemia or . Magnesium occurs mainly in the thick ascending limb (50-70%) via paracellular transport regulated by claudins and the calcium-sensing receptor, and in the (10-15%) via TRPM6 channels influenced by . is proximally (80-90%) via NaPi-IIa cotransporters, downregulated by (PTH) and 23 (FGF23) during to promote excretion and support mineralization. These mechanisms ensure serum levels of magnesium (0.7-1.0 mmol/L) and (0.8-1.5 mmol/L) remain stable.

Acid-base regulation

The urinary system plays a crucial role in maintaining acid-base by reabsorbing (HCO₃⁻) and excreting ions (H⁺), thereby regulating blood within a narrow range of 7.35 to 7.45. This process compensates for daily endogenous acid production from , which generates approximately 50-100 mEq of nonvolatile acids per day in adults on a typical diet. The kidneys achieve net acid excretion primarily through the reclamation of filtered HCO₃⁻ and the secretion of H⁺, which is buffered in the to prevent drastic pH changes. Bicarbonate reabsorption occurs mainly in the proximal tubule, where approximately 80% of the filtered HCO₃⁻ load is reclaimed. This process is indirect and depends on H⁺ secretion into the tubular lumen via the Na⁺/H⁺ exchanger (NHE3), where secreted H⁺ combines with filtered HCO₃⁻ to form carbonic acid (H₂CO₃), which dissociates into CO₂ and H₂O facilitated by luminal carbonic anhydrase IV. The CO₂ diffuses into tubular cells, where intracellular carbonic anhydrase II reforms H₂CO₃, dissociating into H⁺ and HCO₃⁻; the HCO₃⁻ is then transported across the basolateral membrane into the blood via NBC1 (sodium-bicarbonate cotransporter 1). The remaining 10-20% of HCO₃⁻ reabsorption occurs in more distal segments, but the proximal tubule's high-capacity mechanism ensures efficient conservation during normal conditions. Hydrogen ion secretion in the distal nephron, particularly in the collecting duct, is mediated by alpha-intercalated cells to generate new HCO₃⁻ for systemic delivery. These cells express vacuolar on the apical , which actively pumps into the lumen using , creating a steep . Additionally, contributes to secretion, especially under conditions of , by exchanging luminal for intracellular K⁺, thereby supporting both excretion and K⁺ . The secreted is not freely excreted but is buffered to maintain above 4.5, preventing tubular damage. Urinary buffers are essential for handling secreted H⁺, with titratable acids and comprising the primary systems. Titratable acids, mainly (HPO₄²⁻), account for about 90% of titratable acid excretion, where secreted H⁺ converts HPO₄²⁻ to H₂PO₄⁻, allowing up to 20-30 mEq/day of acid disposal at typical urine pH levels. (NH₃) serves as the dominant buffer, produced in the via glutaminase, which deaminates to glutamate and NH₃; glutamate is further metabolized to yield additional NH₃, totaling around 30-50 mEq/day under normal conditions. The NH₃ diffuses into the tubular lumen, trapping H⁺ as non-toxic NH₄⁺, which is excreted; this mechanism can increase substantially during . Net acid excretion, calculated as titratable plus NH₄⁺ minus HCO₃⁻ loss, typically equals 50-100 mEq/day to match metabolic load and maintain balance. In response to , the kidneys enhance net excretion by upregulating ammoniagenesis, H⁺ secretion, and HCO₃⁻ reabsorption, potentially increasing output to 200-300 mEq/day. Conversely, during , net excretion decreases through reduced H⁺ secretion and increased HCO₃⁻ excretion, promoting normalization. This renal compensation integrates with the , where lungs adjust CO₂ levels rapidly (within minutes to hours) to buffer acute changes, while kidneys provide slower but more sustained correction over hours to days.

Blood pressure regulation

The urinary system regulates systemic blood pressure primarily through control of extracellular fluid volume and hormonal modulation of vascular tone and sodium handling. By adjusting renal sodium and water excretion, the kidneys maintain blood volume, while endocrine signals from the kidneys influence vasoconstriction and thirst to fine-tune pressure homeostasis. This integrated function ensures long-term stability of arterial pressure against perturbations in salt intake or fluid status. A central mechanism is the renin-angiotensin-aldosterone system (RAAS), activated when renal perfusion pressure falls, such as during or . Juxtaglomerular cells in the release renin in response to low perfusion, sympathetic stimulation, or reduced sodium delivery to the . Renin cleaves circulating angiotensinogen (produced by the liver) into I, which is then converted to II by (ACE), predominantly in the lungs. II exerts rapid effects by inducing systemic via AT1 receptors, increasing vascular resistance and elevating ; it also stimulates thirst and release to expand plasma volume, and directly enhances sodium reabsorption in the . Further amplifying RAAS, angiotensin II prompts the to secrete aldosterone, which acts on the distal to upregulate epithelial sodium channels (ENaC) and Na+/K+-ATPase activity, thereby increasing sodium and promoting water retention to support . The basic RAAS cascade can be represented as: Renin+Angiotensinogen→Angiotensin I→ACEAngiotensin II→Aldosterone (via adrenal stimulation)\text{Renin} + \text{Angiotensinogen} \rightarrow \text{Angiotensin I} \xrightarrow{\text{ACE}} \text{Angiotensin II} \rightarrow \text{Aldosterone (via adrenal stimulation)}
Add your contribution
Related Hubs
User Avatar
No comments yet.