Altered cavernosal endothelin-B-receptor binding sites in the rabbit model of partial bladder outlet obstruction.

Erectile dysfunction (ED) is a common problem that significantly affects the quality of life. Benign prostatic hyperplasia (BPH) is the commonest known benign proliferative disorder. Recently there has been growing evidence to suggest that patients with high BPH symptom scores have an increased incidence of ED. Endothelin-1 (ET-1) is a potent vasoconstrictor peptide that is thought to play an important role as a modulator of erectile physiology and dysfunction. We investigated whether there are any changes in the density and distribution of ET-1 and its receptor subtypes in the corpora cavernosa (CC) of a rabbit model of partial bladder outflow obstruction (BOO). ET-1, endothelin-A- and -B- (ET(A) and ET(B)) receptor binding sites were primarily localized to the smooth muscle cells (SMC) of the CC and the endothelium lining the cavernosal space. ET(B)-receptor binding sites were significantly decreased (p = 0.04) in the 6-week BOO cavernosal tissue. ET-1 may play a role in the pathophysiology of ED associated with BPH. This may be partly a result of enhanced vasoconstrictor actions and SMC proliferation secondary to a reduction in ET(B)-receptors. Further work is needed to evaluate this possibility.