Igypercontractility and impaired sildenafil relaxations in the BKCa channel model of erectile dysfunction

摘要

Erectile dysfunction (ED) can be elicited by a variety of pathogenic factors, particularly impaired formation of and responsiveness to nitric oxide (NO) and the downstream effectors soluble guanylate cyclase (sGC) and cGMP-depen-. dent protein kinase I (PKGI). One important target of PKGI in smooth muscle is the large-conductance, Ca~(2+)-activated potassium (BKCa) channel. In our previous report (42), we demonstrated that deletion of the BKca channel in mice induced force oscillations and led to reduced nerve-evoked relaxations and ED.