Mechanisms of Ischemia-Induced Cavernosal Smooth Muscle Relaxation Impairment in a Rabbit Model of Vasculogenic Erectile Dysfunction

Abstract

Impairment of endothelium-dependent relaxation by Hch occurs secondary to disruption of the NO formation in cavernosal endothelium. Improvement of endothelium-dependent relaxation by L-arginine may suggest lack of availability of L-arginine in cavernosal tissue from the Hch animals. Impairment of endothelium-dependent and neurogenic relaxation by CCI occurs secondary to disruption of the NO formation due to an alteration in the expression or activity of NOS and increased output of constrictor eicosanoids in cavernosal tissue. These studies show that Hch and atherosclerosis-induced chronic cavernosal arterial insufficiency, beyond decreasing cavernosal perfusion pressure, also adversely affect smooth muscle relaxation mechanisms in cavernosal tissue.

Critical evaluation of the factors influencing erectile function after renal transplantation

“…The mechanism of hypercholesterolemia induced dysfunction of the corporal endothelium may be due to impaired ability of the endothelium to synthesize NO 24 or decreased synthesis or availability of L-arginine. 25 Some authors reported the negative impact of hypercholesterolemia on penile hemodynamics. 19 In the current study, no statistically significant relationship between cholesterol level In contrast with the findings of some authors who reported no correlation between CsA and erectile function 9,19 we found statistically higher incidence of ED among RTR receiving CsA-based immunosuppressive regimens.…”

Corpus Cavernosum from Men with Vasculogenic Impotence Is Partially Resistant to Adenosine Relaxation due to Endothelial A2BReceptor Dysfunction

“…Whether this reflects a reduction of A 2B receptor binding sites or results from impairment of distal effectors pathways needs further investigation. Dysfunctional blood vessels can alter the balance between relaxant and constrictor actions of endogenous prostanoids (Azadzoi et al, 1998;Behr-Roussel et al, 2003). This, together with the reduced NO-mediated component, might explain the difficulty in relaxing HCC strips from vasculogenic ED patients in response to NECA and ACh.…”

Alterations in angiogenic growth factors and neuronal nitric oxide synthase expression in chronic cavernosal ischemia

“…The animal model of arteriogenic ED was developed as previously described. 4,17 Briefly, the CI group underwent bilateral balloon endothelial cell injury of the iliac arteries, received a 0.5% cholesterol diet for 4 weeks, and then a regular diet. Animals were studied at 4, 6, 8, and 16 weeks after the balloon arterial injury.…”