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Am J Physiol Regul Integr Comp Physiol 284: R682-R688, 2003. First published November 7, 2002; doi:10.1152/ajpregu.00349.2002
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Vol. 284, Issue 3, R682-R688, March 2003

Erectile dysfunction in spontaneously hypertensive rats: pathophysiological mechanisms

Delphine Behr-Roussel1, Philippe Chamiot-Clerc1, Jacques Bernabe1, Katell Mevel, Laurent Alexandre1, Michel E. Safar2, and François Giuliano1,3

1 Pelvipharm, Domaine Centre National de Recherche Scientifique, 91190 Gif sur Yvette; 2 Department of Internal Medicine, Broussais Hospital, 75014 Paris; and 3 Groupe de Recherche en Urologie, Unité Propre de Recherche de l'Enseignement Supérieur, Medical University of Paris South, 94275 Le Kremlin Bicêtre Cedex, France

Hypertensive men have a higher prevalence of erectile dysfunction (ED) than the general population. Experimental evidence of ED in hypertensive animals is scarce. This study evaluates the erectile function of spontaneously hypertensive rats (SHR) and age-matched normotensive Wistar-Kyoto rats (WKY) in vivo by the increase in intracavernosal pressure after electrical stimulation of the cavernous nerve (CN) and by isometric tension studies on corporal strips. Frequency-dependent erectile responses to CN stimulations were reduced in SHR. Phenylephrine induced lower corporal contractions in SHR although pD2 values were similar to WKY. Endothelium-dependent relaxations to ACh were impaired significantly in SHR, and indomethacin improved these relaxations in both WKY and SHR, the latter thus reaching values similar to WKY. Corporal relaxations to sodium nitroprusside were enhanced in SHR. Thus a dysfunctional alpha -adrenergic contraction of the corporal smooth muscle, an increased cyclooxygenase-dependent constrictor tone, and/or a defect in endothelium-dependent reactivity are associated with the altered erectile mechanisms in SHR. Drugs targeting endothelial dysfunction may delay the occurrence of ED as a complication of hypertension.

hypertension; endothelial dysfunction; corpus cavernosum


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