A simplified in vitro preparation of the corpus cavernosum as a tool for investigating erectile pharmacology in the rat

Italiano, G.; Calabrò, Antonino; Pagano, Francesco

doi:10.1016/1043-6618(94)80012-x

Cited by 19 publications

(17 citation statements)

References 5 publications

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“…Corpus cavernosum penile tissue muscle strips (partially free of the tunica albuginea) from juvenile (Ϸ3 months old; Ϸ 250 g) male Sprague-Dawley rats (3-5 per preparation) were prepared fresh (within 5 min of killing) as described (24). Tissues were mounted in a 10-ml organ bath chamber and a resting tension of 1.5 mN was applied.…”

Section: Methodsmentioning

confidence: 99%

A role for the melanocortin 4 receptor in sexual function

Ploeg

Martin

Howard

et al. 2002

Proc. Natl. Acad. Sci. U.S.A.

284

207

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By using a combination of genetic, pharmacological, and anatomical approaches, we show that the melanocortin 4 receptor (MC4R), implicated in the control of food intake and energy expenditure, also modulates erectile function and sexual behavior. Evidence supporting this notion is based on several findings: (i) a highly selective nonpeptide MC4R agonist augments erectile activity initiated by electrical stimulation of the cavernous nerve in wild-type but not Mc4r-null mice; (ii) copulatory behavior is enhanced by administration of a selective MC4R agonist and is diminished in mice lacking Mc4r; (iii) reverse transcription (RT)-PCR and non-PCR based methods demonstrate MC4R expression in rat and human penis, and rat spinal cord, hypothalamus, brainstem, pelvic ganglion (major autonomic relay center to the penis), but not in rat primary corpus smooth muscle cavernosum cells; and (iv) in situ hybridization of glans tissue from the human and rat penis reveal MC4R expression in nerve fibers and mechanoreceptors in the glans of the penis. Collectively, these data implicate the MC4R in the modulation of penile erectile function and provide evidence that MC4R-mediated proerectile responses may be activated through neuronal circuitry in spinal cord erectile centers and somatosensory afferent nerve terminals of the penis. Our results provide a basis for the existence of MC4R-controlled neuronal pathways that control sexual function.O ur understanding of the physiology and anatomy of erectile function has advanced considerably in recent years (1-4). Penile erection is a highly coordinated reflex that is subject to modulation at many levels of the neuraxis. Relaxation of smooth muscle fibers of erectile tissue and concomitant dilatation of the arterial supply in the penis produce penile erection. Activation of neurons in the sacral spinal cord triggers activity in the pelvic nerve and, subsequently, the cavernous nerve, which can lead to the release of mediators of vasorelaxation, including nitric oxide. These mediators modulate cyclic nucleotide levels resulting in Ca 2ϩ sequestration and relaxation of smooth muscle fibers of the corpora cavernosa and corpus spongiosum in the shaft of the penis to produce arterial dilatation, engorgement of the penis with blood, and tumescence. Erections can be triggered either by peripheral (tactile) or by central (visual, olfactory, auditory, or imaginative cues) activation of somatic pathways and, as such, are influenced by tonic and phasic activity in the lumbosacral spinal cord and the brain.Five melanocortin heterotrimeric GTP-binding protein (G protein)-coupled receptors have been identified as expressed in different tissues (5, 6). The functional role of each of these five melanocortin receptors is being defined. Rodent and human genetic and pharmacological evidence indicates that activation of melanocortin 4 receptor (MC4R) results in a lean phenotype, whereas inactivation of the MC4R results in obesity (7-10). Recent studies have demonstrated that MTII, a cyclic analogue of ␣-mel...

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Section: Methodsmentioning

confidence: 99%

A role for the melanocortin 4 receptor in sexual function

Ploeg

Martin

Howard

et al. 2002

Proc. Natl. Acad. Sci. U.S.A.

284

207

View full text Add to dashboard Cite

show abstract

“…There is very limited data on the use of the rat as an in vitro model of erectile function. Initial descriptions of two different corpora cavernosal in vitro models have not been followed up by the authors that developed them, 20,21 although other groups have adapted their techniques. 22 ± 25 There is controversy over the role of eNOS in the rat and whether it is a good model of human corpora cavernosal function.…”

Section: Introductionmentioning

confidence: 99%

Endothelial and neuronal-derived nitric oxide mediated relaxation of corpus cavernosal smooth muscle in a rat, in vitro, model of erectile function

et al. 2000

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We set out to establish a simple, reproducible, rat in vitro model of erectile function and to use this to demonstrate the functional importance of both neuronal-and endothelial-derived nitric oxide within this animal.Two corpora cavernosal smooth muscle strips were harvested from sexually mature male Wistar rats and mounted in an organ bath for measurement of isometric tension. Following contraction with noradrenaline the strips were relaxed by the addition of either acetylcholine or sodium nitroprusside. Electrical ®eld stimulation was performed in the presence of atropine and guanethidine. Relaxation responses were repeated in the presence of methylene blue, L-arginine, L-NNA and haemoglobin AE L-arginine.Methylene blue abolishes the relaxation to acetylcholine and EFS; L-NNA and haemoglobin cause a signi®cant impairment in the relaxation response. L-arginine reverses the effect of haemoglobin.In conclusion, the inhibitory, relaxant stimulus of rat corpora cavernosa is due to both neuronal nitric oxide and endothelial-derived nitric oxide released in response to cholinergic stimulation.

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“…PGE-1 mediated vaso-dilation occurs via gap junctions within the penis; additionally PGE-1 inhibits sympathetic activity by acting upon the presynaptic neurons, blocking the release of noradrenaline [70][71][72]. PGE-1 is metabolized by 15-hydroxydehydrogenase and has a blood plasma half-life of less than 1 minute, as liver, kidney, and penile enzymes all contribute to the conversion of PGE-1 to its inactive form [67].…”

Section: Prostaglandin E1mentioning

confidence: 99%