Protection of cavernous tissue in male spontaneously hypertensive rats: Beyond blood pressure control

Abstract

Male erectile dysfunction is increased in prevalence in patients with hypertension. Previous experiments from our group demonstrated morphologic changes in erectile tissue from male spontaneously hypertensive rats (SHR). The aim of the present study was to determine whether blood pressure (BP) control is enough to preserve cavernous tissue from the deleterious effect of arterial hypertension. Eight-week-old male SHR and normotensive Wistar-Kyoto rats (WKY) were studied during 6 months: Group 1 ( n = 10) SHR; group 2 ( n = 10) SHR with 7.5 mg/kg/d candesartan (C); group 3 ( n = 10) SHR with 100 mg/kg/d atenolol (AT); and group 4 ( n = 10) WKY. At the end of the experiment all the animals were killed for microscopic studies. Cavernous tissue was processed by hematoxylin-eosin, Masson's trichrome, monoclonal anti-α-smooth muscle actin, and anticollagen type III. Cavernous smooth muscle (CSM) and vascular smooth muscle (VSM) from cavernous arteries and the amounts of collagen type III were evaluated. At the end of the experiment, SHR with C and AT showed similar control in BP (group 2: 131.3 ± 5.5 mm Hg; group 3: 136.5 ± 2.9 mm Hg) compared with untreated SHR (group 1: 199.6 ± 5.1 mm Hg). However, animals with C presented significantly lower values ( P < .01) of CSM layer in cavernous space and VSM in cavernous arteries ( P < .01), and lower amounts of collagen type III ( P < .01) compared to SHR with AT and untreated SHR. We conclude that C provides a significant protective role against structural changes in vessels as well as in cavernous spaces of the erectile tissue, caused by arterial hypertension in SHR, beyond BP control.