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Clitoral erection
Clitoral erection
Clitoral erection
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Left image: Mild sexual arousal. Right image: Strong sexual arousal with erection of the vestibular bulbs under the skin on both sides of the vaginal opening and exposed clitoral glans.

Clitoral erection (also known as clitoral tumescence or female erection)[1][2] is a physiological phenomenon where the clitoris becomes enlarged and firm.

Clitoral erection is the result of a complex interaction of psychological, neural, vascular, and endocrine factors, and is usually, though not exclusively, associated with sexual arousal. Erections should eventually subside, and the prolonged state of clitoral erection even while not aroused is a condition that could become painful.[3] This swelling and shrinking to a relaxed state seems linked to nitric oxide's effects on tissues in the clitoris, similar to its role in penile erection.[4]

Physiology

[edit]
The internal anatomy of the human vulva, with the clitoral hood and labia minora indicated as lines.

The clitoris is the homolog to the penis in the male. Similarly, the clitoris and its erection can subtly differ in size.[5]

The visible part of the clitoris, the glans clitoridis, varies in size from a few millimeters to one centimeter and is located at the front junction of the labia minora (inner lips), above the opening of the urethra. It is covered by the clitoral hood.

Any type of motion can increase blood flow to this organ and this results in increased secretions which lubricate the vagina. There are many ways to stimulate the clitoris.

Clitoral erection occurs when the corpora cavernosa, two expandable erectile structures, become engorged with blood. This may result from any of various physiological stimuli, including sexual arousal. During sexual arousal, arterial blood flow to the clitoris is increased, and trabecular smooth muscle within the clitoris relaxes allowing blood to engorge the erectile tissues. The ischiocavernosus and bulbospongiosus muscles contract to compress the dorsal vein of the clitoris to stop drainage of the clitoris, trapping the blood.[6] The erectile tissues are composed of endothelium-lined vascular spaces in a trabecular matrix, with the endothelium-lined vascular spaces surrounded by smooth muscle capable of contraction and relaxation.

During sexual arousal, arterial blood flow to the clitoris is increased, and within the clitoris, the arteries further branch to supply the erectile tissues. The trabecular smooth muscles of the erectile tissue relax increasing blood flow to fill the vascular spaces, and expanding the erectile tissues until they are fully engorged with blood.[7] The ischiocavernosus and bulbocavernosus muscles contract, compressing the dorsal vein of the clitoris. This compression of the vein restricts drainage of the erectile structures, trapping the blood.[8] This process stretches the tunica albuginea. As a result, the clitoris becomes tumescent to accommodate the increased intracavernosous pressure. The tunica albuginea of the clitoris is made up of one layer making it more elastic than the tunica albuginea of the penis, which is composed of two layers.[9] Erick Janssen (2007) elaborates on this reporting that "the corpora cavernosa of the clitoris are essentially similar to that of the penis except that there is no subalbugineal layer interposed between the tunica albuginea and the erectile tissue. In the penis, this[10] tissue engorges with blood during sexual arousal and becomes compressed against the unyielding tunica, creating penile rigidity – a true erection. The lack of this plexus in the clitoris indicates that while the organ can become tumescent or engorged, it cannot, like the penis, become stiffly erect. The clitoris thus does not become erect with sexual excitement, but engorged."[10] In addition, the tunica albuginea around the glans is thinner than around the shaft in both the clitoris and penis. This gives the glans less firmness relative to the shaft. The extrusion of the glans clitoridis and thinning of the skin enhances sensitivity to physical contact. After a female has orgasmed, the erection usually ends, but this may take time.

Medical conditions

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Clitoral priapism

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Priapism, while more common in males, is a condition that can also affect the clitoris.[3] Symptoms include painful engorgement, swelling, and pain in the area around the clitoris.[11]

Other animals

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Among capuchin monkeys, clitoral erection is possible and makes the clitoris more visible than in its relaxed state where it is hidden by a preputial fold.[12]

See also

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Notes

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References

[edit]
Revisions and contributorsEdit on WikipediaRead on Wikipedia

Clitoral erection

View on Grokipedia
from Grokipedia
Clitoral erection is a physiological in which the , the primary erectile organ in anatomy, becomes enlarged, firm, and more sensitive due to increased blood flow during , serving as the homolog to penile . This process involves the engorgement of the clitoral corpora cavernosa with , leading to that enhances sexual pleasure and facilitates . The erection progresses through three distinct phases: latent (initial subtle filling), turgid (full swelling and protrusion), and rigid (maximal firmness and retraction of the shaft into the prepuce). The is a Y-shaped structure measuring approximately 7-13 cm in length, comprising the visible , an internal body or shaft, and paired crura that extend along the pubic rami, all encased in similar to the penile corpora cavernosa. During , the extrudes from beneath the , while the internal components expand, contributing to overall genital that also affects the and . Unlike the , the lacks a and focuses solely on sensory and erectile functions, with approximately 10,000 nerve fibers innervating the for heightened tactile sensitivity. This underscores the clitoris's central role in sexual response, independent of vaginal penetration. The mechanism of clitoral erection is mediated primarily by the parasympathetic nervous system via the pelvic nerves, which release nitric oxide (NO) from nerve endings and endothelial cells within the clitoral vasculature. NO diffuses into smooth muscle cells of the helicine arterioles and corpora cavernosa, activating guanylate cyclase to produce cyclic guanosine monophosphate (cGMP), which lowers intracellular calcium levels and induces relaxation, thereby increasing arterial inflow and trapping blood through venous compression. This process is estrogen-dependent for optimal vascular health and can be disrupted by conditions like atherosclerosis or hormonal imbalances, potentially leading to erectile dysfunction. Notably, the absence of a refractory period post-orgasm allows for multiple clitoral erections and orgasms in a single session, distinguishing it from male physiology.

Anatomy

Clitoral structure

The is a complex erectile organ in the female external genitalia, primarily composed of the , body (or shaft), and two crura, all supported by the corpus cavernosum clitoridis, which is the main erectile tissue homologous to the corpora cavernosa of the . The clitoridis forms the visible, external tip, typically covered by a prepuce and richly endowed with endings, serving as the primary site of stimulation. The body extends internally from the as a cylindrical containing paired corpora cavernosa, while the crura represent the diverging proximal portions that attach to the ischiopubic rami, forming the "legs" of the organ. Adjacent to the crura are the , paired erectile structures composed of corpus spongiosum tissue homologous to the penile bulb, which encircle the vaginal opening and contribute to engorgement during , though they are distinct from the proper. In terms of dimensions and variability, the external measures approximately 4-6 mm in length and 3-4 mm in width on average, but the total clitoral structure, including the internal body and crura, extends 7-12 cm in length, exhibiting a wishbone-like configuration that flanks the urethral walls and . This internal extension varies significantly among individuals, influenced by factors such as age, hormonal levels, and genetic differences, with some studies reporting crura lengths of up to 9 cm each. Histologically, the corpus cavernosum clitoridis consists of a spongy network of trabeculae—strands of and —that enclose vascular sinusoidal spaces, allowing for blood accumulation and tissue expansion. These trabeculae are covered by a fibrous tunica albuginea, similar to that in penile , and the overall composition supports rigidity upon vascular filling while maintaining flexibility in the flaccid state. Embryologically, the arises from the , an undifferentiated phallic structure present in both sexes around the 5th week of , which in females differentiates under the influence of anti-androgenic signals and to form the , body, and crura without significant elongation. The develop separately from the , completing the erectile framework by the 12th week.

Vascular and neural components

The arterial supply to the primarily derives from the , a branch of the anterior division of the . This artery bifurcates into the dorsal artery of the clitoris, which supplies the overlying skin and fascia, and the deep (cavernosal) artery of the clitoris, which penetrates the tunica albuginea to vascularize the corpora cavernosa. These vessels enable the engorgement of during by facilitating increased blood inflow. Venous drainage occurs mainly through the dorsal veins of the , including paired deep dorsal veins located medial to the arteries and an unpaired superficial dorsal vein positioned more superficially. These veins converge to empty into the internal pudendal veins, which ultimately drain into the , while some superficial tributaries connect to the external pudendal veins leading to the . This drainage system supports the potential for temporary venous congestion that contributes to tissue rigidity. Neural innervation of the clitoris involves both somatic and autonomic components. The somatic sensory supply arises from the (S2-S4), which gives off the ; this terminal branch travels along the dorsal surface, bifurcating into multiple fascicles that terminate in the with approximately 10,000 myelinated and unmyelinated nerve fibers, providing exquisite tactile sensitivity. Autonomic innervation includes parasympathetic fibers from the (S2-S4), which promote in the erectile tissues via neurotransmitter release, such as , at varicosities along the . Lymphatic drainage from the follows vessels that accompany the venous pathways, primarily directing lymph to the , with some efferents reaching deep inguinal nodes and pelvic nodes via connections along the internal pudendal vessels.

Erection mechanism

Clitoral begins with a vasocongestive process triggered by parasympathetic neural stimulation during , which promotes the release of (NO) from non-adrenergic non-cholinergic nerve endings and endothelial cells within the clitoral vasculature. This NO diffuses into cells of the corpora cavernosa, activating soluble to increase (cGMP) levels, which in turn leads to protein kinase G (PKG)-dependent relaxation of the . The relaxation causes arterial dilation, allowing increased blood inflow into the sinusoidal spaces of the while restricting venous outflow through compression of subtunical venules, resulting in tissue engorgement and . The erection progresses through distinct phases: initial tumescence involves swelling of the glans and shaft due to rapid blood engorgement, followed by full with expansion of the internal crura, achieving rigidity as relaxation is sustained. This phased response is mediated by sustained NO/cGMP signaling, which hyperpolarizes the membrane via activation of large-conductance calcium-activated (BKCa) channels, reducing calcium influx and maintaining the relaxed state. Detumescence occurs upon cessation of arousal, involving sympathetic nervous system activation that releases norepinephrine, inducing vasoconstriction through alpha-adrenergic receptors and restoring smooth muscle tone to facilitate venous drainage and return blood flow to baseline. Quantitative aspects include increased clitoral blood flow during peak arousal, driven by the hemodynamic changes, with intracavernosal pressure rising in the erectile tissues to support rigidity. Recent 2025 biophysical models of clitoral emphasize the role of ion channels, such as L-type voltage-gated calcium channels and BKCa channels, in regulating and calcium dynamics, providing a framework for understanding the cellular basis of NO-mediated relaxation and potential therapeutic targets for disorders.

Regulatory factors

Clitoral erection is regulated by a complex interplay of neural, hormonal, and psychological factors that initiate and modulate the process. Neural regulation involves both central and peripheral pathways. Central pathways originate in the and , where sensory and emotional inputs are integrated to activate autonomic centers responsible for . The paraventricular nucleus of the coordinates these responses by releasing oxytocin, which facilitates genital and erection. At the spinal level, reflex arcs are mediated via the , which transmits sensory feedback from the clitoral to the sacral (S2-S4), triggering parasympathetic efferents that promote and . Hormonal influences significantly affect clitoral erectile function by maintaining vascular integrity and sensitivity. supports endothelial health in clitoral corpora cavernosa, ensuring adequate production for during . enhances clitoral relaxation through the -cyclic GMP pathway, thereby improving erectile capacity. In contrast, progesterone exerts inhibitory effects during the of the , reducing . Psychological factors play a crucial role in initiating clitoral erection, as is heavily dependent on cognitive and emotional stimuli such as anticipation, fantasy, and relational context. These elements are processed through the and integrated at the paraventricular nucleus, where they trigger descending signals to amplify genital responses. Disruptions in mood or stress can inhibit this pathway, underscoring the mind-body linkage in female sexual physiology. Age-related changes, particularly post-menopause, alter regulatory dynamics due to declining levels, which reduce clitoral vascular health and erectile responsiveness, as evidenced by diminished genital blood flow and sensitivity. This hypoestrogenic state leads to atrophic changes in clitoral tissue, impairing the erectile process. Pharmacological interactions can modulate clitoral erection, notably through phosphodiesterase type 5 (PDE5) inhibitors like , which enhance blood flow by preventing cyclic GMP degradation in vascular , thereby promoting engorgement even in the absence of direct . Clinical studies confirm increased clitoral arterial inflow with in postmenopausal women, supporting its role in addressing deficits.

Pathophysiology

Associated disorders

Female sexual interest/ disorder (FSIAD) is a common condition characterized by the persistent or recurrent inability to achieve or maintain sufficient sexual excitement, leading to reduced genital sensation and , which impairs clitoral engorgement and . It affects approximately 9-26% of women in the general population, with higher rates observed in specific subgroups such as those with chronic illnesses. Psychological factors, including depression, anxiety, and relationship distress, also significantly contribute to FSIAD, often interacting with physiological causes. These difficulties often stem from vascular insufficiency, which limits blood flow to the clitoral corpora cavernosa, or neuropathy, which diminishes sensory feedback necessary for initiation. Diabetes mellitus frequently contributes to FSIAD through , which reduces clitoral sensation and elevates the threshold for stimulation, thereby hindering erectile response. In women with , sexual dysfunction prevalence reaches 20-80%, with neuropathy directly correlating to deficits by impairing neural transmission from the . exacerbates this by causing arterial insufficiency, restricting the required for clitoral blood influx and erection. Iatrogenic causes, such as pelvic surgeries (e.g., or repairs), can damage clitoral nerves or alter vascular supply, leading to postoperative impairment in 13-37% of cases. Hormonal imbalances, particularly hypoandrogenism, diminish clitoral erectile capacity by reducing androgen-mediated vascular and tissue maintenance. In menopausal women, estrogen decline combined with relative promotes genitourinary of menopause (GSM), which can include clitoral characterized by shrinkage and decreased responsiveness due to diminished blood flow and tissue elasticity. GSM affects approximately 50% of postmenopausal women, often manifesting as reduced and . Diagnosis of FSIAD-related clitoral dysfunction typically involves tools like , which measures clitoral pulse amplitude and blood volume changes during stimulation to quantify erectile impairment. This objective assessment helps differentiate vascular from neurologic causes by evaluating in the clitoral arteries. Treatment strategies target underlying etiologies; , including topical estrogen or testosterone, improves clitoral vascularization and sensation in hypoandrogenic cases. Lifestyle interventions, such as and exercise to bolster cardiovascular health, mitigate vascular insufficiency. Topical vasodilators, like alprostadil or creams, promote localized clitoral engorgement, with studies showing significant improvements in and satisfaction rates.

Clitoral priapism

Clitoral is a rare defined as a prolonged, painful of the lasting more than 4 hours, unrelated to or stimulation. It parallels penile in its and is classified into two main types: low-flow (ischemic) , caused by impaired venous outflow leading to and tissue hypoxia, and high-flow (non-ischemic) , resulting from unregulated arterial inflow without significant ischemia. A variant involves recurrent, intermittent episodes, though less commonly reported in clitoral cases. The etiology of clitoral often involves disruption of normal vascular regulation in the and vein system. Common causes include trauma to the perineal or pudendal vessels, such as from aggressive or , which can create arteriovenous fistulas leading to high-flow states. Medications, particularly antidepressants like and , or anticoagulants, may induce low-flow by altering serotonergic or activity. Hematologic disorders, such as , contribute through vaso-occlusive crises, while rare triggers include post-appendectomy inflammation. Symptoms typically manifest as persistent clitoral engorgement and swelling, accompanied by throbbing or searing pain and tenderness, which can disrupt daily activities and sexual function. Prolonged untreated episodes risk tissue ischemia, potentially causing fibrosis, clitoromegaly, or chronic pain. Diagnosis relies on a detailed history and physical exam, with color Doppler ultrasound essential to differentiate types by flow patterns—high resistive index in low-flow cases versus low resistance in high-flow. MRI provides additional assessment of internal structures and rules out compressive lesions. Management prioritizes rapid intervention to prevent complications, beginning with conservative measures such as application, , and oral sympathomimetics like (30-60 mg every 6-8 hours) to promote . For persistent cases, intracavernosal aspiration of blood or injection of alpha-agonists like is performed under . Surgical shunting, such as cavernoglanular , is reserved for refractory low-flow . Case reports from the demonstrate favorable outcomes, including resolution via medication discontinuation in drug-induced cases and low-intensity extracorporeal (Li-ESWT) for chronic high-flow after six sessions.

Comparative Biology

In non-human animals

In non-human mammals, clitoral erection exhibits physiological similarities to human processes, often involving vascular engorgement and neural activation during reproductive behaviors. In such as the rhesus monkey (Macaca mulatta), clitoral engorgement occurs alongside labial swelling and during sexual and estrus, driven by hormonal influences that enhance genital blood flow and tissue responsiveness. Similarly, in rodents like female rats, clitoral vascular responses include increased blood flow to the corpus cavernosum following tactile or neural stimulation, mediated by (NO) pathways that promote relaxation and . These homologous structures highlight conserved mechanisms across mammals, where clitoral erection facilitates sensory feedback during mating. Non-mammalian species display more limited analogs to clitoral erection, with reduced but evidence of tied to reproductive displays. In birds, such as wild turkeys, females exhibit swelling of the cloacal opening during mating season, involving protrusion that may signal receptivity, though lacking the cavernosal architecture seen in mammals. Reptilian females, including those in orders like , possess hemiclitores—paired clitoral analogs—with and nerve bundles; recent studies (as of 2022) have identified these in snakes, suggesting supports sensory functions during , though less specialized than in mammals. Animal models have been instrumental in elucidating clitoral erection mechanisms, particularly through pharmacological investigations. In rabbits, NO-mediated leads to clitoral corpus cavernosum relaxation via nitrergic , as demonstrated by non-adrenergic, non-cholinergic responses inhibited by NOS blockers, providing insights into inhibitors for enhancing genital blood flow. Dog models similarly show NO/cGMP pathway involvement in clitoral and vaginal , with potentiating pelvic nerve-evoked blood flow increases, informing translational therapies for disorders. These studies underscore the role of endothelial-derived NO in vascular dilation across species. Behavioral observations link clitoral erection to reproductive postures in , enhancing motivational aspects of mating. In female rats, clitoral engorgement correlates with —a reflexive arching posture elicited during mounting—where genitosensory increases vaginal and clitoral blood flow, measurable via photoplethysmography to quantify intensity. This association reinforces copulatory pacing and reward, as clitoral tactile input modulates solicitational behaviors. Recent biophysical research in porcine models advances understanding of female genital arousal dynamics. In 2024 studies, ex-vivo analyses of porcine perineal tissues, including clitoral analogs, revealed biomechanical properties of contraction and relaxation under hormonal simulation, modeling vasocongestive responses with implications for in arousal research. These findings complement earlier mammalian data by quantifying viscoelastic behaviors in larger-animal vasculature.

Evolutionary perspectives

The clitoris is considered evolutionarily homologous to the , both arising from the indifferent in mammalian embryos, which is sensitive to such as (DHT). In the absence of significant androgen exposure, the develops into the clitoris, while DHT promotes its elongation and differentiation into the penis, highlighting a shared developmental pathway conserved across mammals. Evolutionary theories propose that clitoral erection enhances sexual pleasure and facilitates , potentially strengthening pair bonding and influencing by rewarding interactions with compatible partners. This mechanism may signal genetic quality or commitment in long-term relationships, as higher orgasm frequency correlates with mate retention and satisfaction in human studies. In comparative mammalian evolution, the loss of the (penis bone) in humans—the only great ape without one—correlates with a greater reliance on vascular mechanisms for erection, including clitoral engorgement, possibly linked to shifts toward prolonged copulation and monogamous mating strategies. Phylogenetic analyses indicate this loss occurred at least once in the hominid lineage, around the time of approximately 1.9 million years ago, coinciding with the emergence of social monogamy and inferred from changes in reproductive behavior. Controversies persist regarding whether clitoral erection and female represent a direct or a developmental of male pathways. Proponents of the view argue it actively promotes pair bonding and mate selection, while advocates contend its variability across individuals undermines selective pressure, though clitoral homology provides a mechanistic link to penile function. Recent genomic studies post-2022 have revealed co-option of ancestral regulatory landscapes involving clusters in the evolution of mammalian genitalia, where posterior influence patterning of the and its differentiation into erectile structures across species. These findings underscore conserved cis-regulatory elements that drive genital diversification, linking embryonic development to broader evolutionary transitions in reproductive anatomy.

References

  1. https://pubmed.ncbi.nlm.nih.gov/23169570/
  2. https://pubmed.ncbi.nlm.nih.gov/36763957/
  3. https://www.bumc.bu.edu/sexualmedicine/physicianinformation/biology-of-female-sexual-function/
  4. https://pmc.ncbi.nlm.nih.gov/articles/PMC12433954/
  5. https://www.ncbi.nlm.nih.gov/books/NBK547703/
  6. https://pmc.ncbi.nlm.nih.gov/articles/PMC3175415/
  7. https://pubmed.ncbi.nlm.nih.gov/1603495/
  8. https://pubmed.ncbi.nlm.nih.gov/25727497/
  9. https://onlinelibrary.wiley.com/doi/10.1002/ca.22177
  10. https://www.ncbi.nlm.nih.gov/books/NBK557601/
  11. https://pmc.ncbi.nlm.nih.gov/articles/PMC6234061/
  12. https://www.kenhub.com/en/library/anatomy/clitoris
  13. https://www.bumc.bu.edu/sexualmedicine/physicianinformation/female-genital-anatomy/
  14. https://news.ohsu.edu/2022/10/27/pleasure-producing-human-clitoris-has-more-than-10-000-nerve-fibers
  15. https://www.kenhub.com/en/library/anatomy/pelvic-splanchnic-nerves
  16. https://www.ncbi.nlm.nih.gov/books/NBK557639/
  17. https://www.kenhub.com/en/library/anatomy/inguinal-lymph-nodes
  18. https://doi.org/10.3389/fphys.2025.1626675
  19. https://pubmed.ncbi.nlm.nih.gov/15333581/
  20. https://pmc.ncbi.nlm.nih.gov/articles/PMC6908863/
  21. https://pmc.ncbi.nlm.nih.gov/articles/PMC2740385/
  22. https://pmc.ncbi.nlm.nih.gov/articles/PMC5340504/
  23. https://pubmed.ncbi.nlm.nih.gov/11426351/
  24. https://www.sciencedirect.com/science/article/abs/pii/S1743609516304672
  25. https://www.researchgate.net/publication/299941164_Within-cycle_fluctuations_in_progesterone_negatively_predict_changes_in_both_in-pair_and_extra-pair_desire_among_partnered_women
  26. https://www.sciencedirect.com/science/article/abs/pii/S1521690X0700036X
  27. https://www.mdpi.com/1648-9144/55/9/559
  28. https://pmc.ncbi.nlm.nih.gov/articles/PMC1480594/
  29. https://www.sciencedirect.com/science/article/pii/S0015028206000859
  30. https://www.ncbi.nlm.nih.gov/books/NBK603746/
  31. https://www.bumc.bu.edu/sexualmedicine/physicianinformation/epidemiology-of-fsd/
  32. https://www.uptodate.com/contents/overview-of-sexual-dysfunction-in-females-epidemiology-risk-factors-and-evaluation
  33. https://med.stanford.edu/obgyn/divisions/gyn/fsm/arousal_disorder.html
  34. https://diabetesjournals.org/clinical/article/43/3/420/157712/Addressing-Sexual-Dysfunction-in-Women-With-Type-1
  35. https://nursing.ceconnection.com/ovidfiles/00006205-201811000-00007.pdf
  36. https://www.ahajournals.org/doi/10.1161/CIRCULATIONAHA.113.004846
  37. https://www.europeanurology.com/article/S0302-2838%2806%2900339-3/fulltext
  38. https://pmc.ncbi.nlm.nih.gov/articles/PMC8572206/
  39. https://www.healthline.com/health/womens-health/clitoral-atrophy
  40. https://www.mayoclinicproceedings.org/article/S0025-6196(11)60314-5/fulltext
  41. https://pubmed.ncbi.nlm.nih.gov/19473468/
  42. https://www.sciencedirect.com/science/article/abs/pii/S1743609520301211
  43. https://www.uspharmacist.com/article/female-sexual-dysfunction-from-causality-to-cure
  44. https://journals.sagepub.com/doi/10.2217/17455057.2.3.331
  45. https://pmc.ncbi.nlm.nih.gov/articles/PMC8766260/
  46. https://pmc.ncbi.nlm.nih.gov/articles/PMC11630007/
  47. https://www.sciencedirect.com/science/article/abs/pii/S2050052115301086
  48. https://pmc.ncbi.nlm.nih.gov/articles/PMC10448556/
  49. https://pubmed.ncbi.nlm.nih.gov/36112421/
  50. https://www.utsc.utoronto.ca/~burton/burt-web/climax.pdf
  51. https://www.researchgate.net/publication/12340589_Increases_in_clitoral_and_vaginal_blood_flow_following_clitoral_and_pelvic_plexus_nerve_stimulations_in_the_female_rat
  52. https://pmc.ncbi.nlm.nih.gov/articles/PMC2755016/
  53. https://www.mossyoak.com/our-obsession/blogs/turkey/wild-turkey-mating-behavior-courtship-breeding-and-reproductive-insights
  54. https://royalsocietypublishing.org/doi/10.1098/rspb.2022.1702
  55. https://pubmed.ncbi.nlm.nih.gov/9886752/
  56. https://www.semanticscholar.org/paper/Vardenafil-enhances-clitoral-and-vaginal-blood-flow-Angulo-Cuevas/d69ab32064f1b810e9f7cea8d95cf27c4242a4bf
  57. https://www.frontiersin.org/journals/behavioral-neuroscience/articles/10.3389/fnbeh.2019.00187/full
  58. https://pmc.ncbi.nlm.nih.gov/articles/PMC454387/
  59. https://pubmed.ncbi.nlm.nih.gov/38908107/
  60. https://www.preprints.org/manuscript/202403.1690/v1
  61. https://www.cambridge.org/core/books/cambridge-handbook-of-evolutionary-perspectives-on-sexual-psychology/adaptive-value-of-womens-orgasm/031E031CB69E0C37107EE2676DF4EB35
  62. https://pmc.ncbi.nlm.nih.gov/articles/PMC10303466/
  63. https://www.science.org/content/article/why-humans-lost-their-penis-bone
  64. https://royalsocietypublishing.org/doi/10.1098/rspb.2016.1736
  65. https://pmc.ncbi.nlm.nih.gov/articles/PMC10108237/
  66. https://www.researchgate.net/publication/6994487_The_Evolution_of_Female_Orgasm_Adaptation_or_Byproduct
  67. https://pmc.ncbi.nlm.nih.gov/articles/PMC10996561/
  68. https://www.biorxiv.org/content/10.1101/2024.03.24.586442v1.full.pdf
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