THE LOSS OF ALPHA-ADRENERGIC EFFECT DURING THE ERECTILE RESPONSE IN THE LONG-TERM DIABETIC RAT

Citation
Tm. Mills et al., THE LOSS OF ALPHA-ADRENERGIC EFFECT DURING THE ERECTILE RESPONSE IN THE LONG-TERM DIABETIC RAT, Journal of andrology, 19(4), 1998, pp. 473-478
Citations number
41
Categorie Soggetti
Andrology
Journal title
ISSN journal
01963635
Volume
19
Issue
4
Year of publication
1998
Pages
473 - 478
Database
ISI
SICI code
0196-3635(1998)19:4<473:TLOAED>2.0.ZU;2-Z
Abstract
The present study was designed to investigate the effect of long-term, streptozotocin-induced diabetes on the erectile response in the labor atory rat. Mean arterial blood pressure (MAP) and intracavernosal bloo d pressure within the erectile tissue (CCP) were continuously monitore d during erection elicited by stimulation of the autonomic innervation of the penis. MAP and CCP were also measured during administration of two drugs: nitroglycerin, a nitric oxide donor drug and phenylephrine , an alpha-adrenergic agonist. The results of these studies show that during graded electrical stimulation of the ganglion, the overall magn itude of the erectile response was greater in the diabetic rats than i n untreated control animals. Neither diabetic nor control animals resp onded significantly to infusion of nitroglycerin. However, diabetic ra ts and control rats responded very differently to administration of ph enylephrine; in the control rats, this alpha agonist caused a sharp de cline in CCP as the cavernosal vessels constricted in response to the drug. The same dose of phenylephrine had no discernible effect on CCP in the diabetic animals. This loss of a responsiveness may be confined to the penile circulation because MAP was elevated to approximately t he same extent in both groups. Taken together, these results show that long-term diabetes leads to a failure of alpha-adrenergic responsiven ess in the cavernosal circulation. The greater erectile response to ga nglionic stimulation in the diabetic animals is likely due to the loss of response to endogenous norepinephrine.