Neural control of penile erection in the rat

Giuliano, François; Rampin, Olivier; Bernabé, Jacques; Rousseau, Jean-Paul

doi:10.1016/0165-1838(95)00025-s

Cited by 136 publications

(143 citation statements)

References 33 publications

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“…9,10 The small, sharp increases of the ICP superimposed to the ICP rises ( Figure 3A) observed after apomorphine injection are likely due to contractions of the ischiocavernosus muscles. 19 In physiological conditions, such contractions, which are only effective after engorgement by blood of the penis, enhances penile rigidity to allow ef®cient intromission. It is tempting to link the putative activity of the ischiocavernosus muscle observed after apomorphine i.v.…”

Section: Discussionmentioning

confidence: 99%

Spinal proerectile effect of apomorphine in the anesthetized rat

et al. 2001

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Considering the presence of dopaminergic receptors in the lumbosacral spinal cord, we tested whether apomorphine could exert a proerectile effect by acting at the spinal level. Intracavernous (ICP) and blood pressures (BP) were measured in anesthetized rats. ICP rises were quanti®ed (duration, percentage of ICPmaximumameanBP (ICPmaxaBP 6 100), area under ICP curve (AUCaBP) and sum of AUCaBP after intravenous (i.v.) and intrathecal (i.t.) injections of apomorphine alone or in presence of i.t. oxytocin (10 ng). Both 10 and 30 m mg i.v. apomorphine dosings elicited erectile events evidenced by ICP rises. Upon the 30 m mg i.v. injection, duration of ICP rises were increased from 25 AE 10 to 69 AE 18 s (P`0.001), ICPmaxaBP 6 100 from 21 AE 3 to 50 AE 14% (P 0.001), AUCaBP from 3 AE 1 to 14 AE 6 s (P 0.002) and sum of AUCaBP from 5 AE 7 to 34 AE 35 s (P 0.021). Upon 30 m mg i.t. injections of apomorphine at the lumbosacral level, the number of ICP rises was increased from 0.2 AE 0.4 to 3.0 AE 1.5, ICPmaxaBP 6 100 from 16 AE 9 to 43 AE 12 and sum of AUCaBP from 1 AE 3 to 31 AE 15 s compared to vehicle injection (P`0.05 for all parameters). Injection of 30 m mg i.v. or i.t. apomorphine non-signi®cantly enhanced the number and amplitude of the ICP rises induced by 10 ng i.t. oxytocin. However, the enhancement of the amplitude of the ICP rises elicited by i.t. oxytocin was more pronounced with i.t. apomorphine than with i.v. apomorphine. These results suggest the existence of a spinal site of action for apomorphine which may (1) participate to generation of erection and (2) exerts a facilitator effect on erection of supraspinal origin.

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Section: Discussionmentioning

confidence: 99%

Spinal proerectile effect of apomorphine in the anesthetized rat

et al. 2001

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“…Both preganglionic parasympathetic neurons and pudendal motoneurons contribute to erection in physiological conditions. 9,11 The contribution of the sympathetic out¯ow has also been recently examined. In rats preganglionic sympathetic neurons are present in the intermediolateral cell column of the T13-L2 spinal cord.…”

Section: Spinal Nuclei That Control Penile Erectionmentioning

confidence: 99%

“…Activation of the lumbosacral parasympathetic pathways, issued from the sacral segments of the spinal cord in a variety of mammals including humans, and from the L6-S1 spinal cord in rats, leads to penile erection. 9 Parasympathetic preganglionic neurons, whose axons run in the pelvic nerves, are present in the sacral parasympathetic nucleus, i.e. in rats the intermediolateral cell column of the L6-S1 spinal cord.…”

Section: Spinal Nuclei That Control Penile Erectionmentioning

confidence: 99%

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Central noradrenergic control of penile erection

Giuliano

Rampin

2000

Int J Impot Res

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Penile erection is completely dependent on commands from the central nervous system. Spinal centers controlling penile erection are located in the thoracolumbar and lumbosacral spinal cord. These centers are activated by information from the periphery and supraspinal nuclei so as to elicit penile erection in a variety of physiological contexts. A small number of nuclei including the locus coeruleus located in the pons sends noradrenergic ®bers to the forebrain and spinal cord, including those areas controlling penile erection. Recent morphological techniques such as in situ hybridization and autoradiography using radioligand binding permit investigation of the brain and spinal pathways utilizing alpha adrenoceptor subtypes. Furthermore, pharmacological experiments suggest a modulatory role for noradrenaline in the control of penile erection either in the brain or in the spinal cord. The most robust evidence is that central inhibition of alpha-2 adrenoceptors facilitates sexual function. Taken together, the data propose new directions in the physiological exploration of penile erection and the therapeutic approach of erectile dysfunction.

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“…1,2 During erectile stimulation (predominantly through activation of non-adrenergicanon-cholinergic nerves) the release of nitric oxide (NO) initiates cavernosal smooth muscle relaxation, resulting ultimately in increased CCP and penile erection. 3 ± 6 Although this NOmediated pathway is thought to be the principal mechanism leading to erection, evidence also exists implicating the role of other vasodilators (acetylcholine 3,4 and vasoactive intestinal peptide 7 ± 9 ), as well as various vasoconstrictors (norepinephrine 10 ± 13 and endothelin-1 14 ± 16 ), in the regulation of cavernosal tone. This paper will brie¯y outline the role of some of these known players, however, the bulk of this paper will be centered around describing a role for a novel calcium-sensitizing pathway, involving the small G-protein RhoA and a downstream target, Rho-kinase, in the maintenance of cavernosal vasoconstriction.…”

Section: Introductionmentioning

confidence: 99%

RhoA/Rho-kinase: a novel player in the regulation of penile erection

2001

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Current research has centered around the role of nitric oxide in the stimulation of cavernosal vasodilation and erection. However, recent evidence from our lab details the importance of endogenous vasoconstrictor mechanisms in maintaining a¯accid penile state, and further demonstrates that the inhibition of endogenous vasoconstriction is suf®cient to stimulate erection in a rat model. In this article, we suggest inhibition of endogenous vasoconstriction as a potential therapeutic avenue in the treatment of erectile dysfunction. We also speculate on potential physiologic mechanisms by which endogenous vasoconstriction is inhibited in order for arousalinitiated vasorelaxation, and erection, to occur.

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Neural control of penile erection in the rat

Cited by 136 publications

References 33 publications

Spinal proerectile effect of apomorphine in the anesthetized rat

Spinal proerectile effect of apomorphine in the anesthetized rat

Central noradrenergic control of penile erection

RhoA/Rho-kinase: a novel player in the regulation of penile erection

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