RYANODINE-SENSITIVE INTRACELLULAR CA2+ STORES IN ISOLATED RABBIT PENILE ERECTILE TISSUE

Norepinephrine release from adrenergic nerve terminals leads to a rise in intracellular Ca2+, which promotes penile smooth muscle contractio n and detumescence. Ca2+ sources are the extracellular space and sarco plasmic Ca2+ stores. To elucidate the role of intracellular stores str ips from rabbit erectile tissue were investigated in an organ bath stu dy. Contractions were elicited by phenylephrine (PE) and electrical st imulation. Incubation in Ca2+-free solution as well as exposure to nif edipine did not abolish electrical or PE-induced contraction. Ryanodin e (10(-5) mol/l), a functional blocker of sarcoplasmic Ca2+ channels, significantly reduced PE response. In the presence of caffeine (10(-3) mol/l) the effect was significantly enhanced. Addition of nifedipine nearly abolished the contraction. These results provide evidence for i ntracellular Ca2+ pools in cavernosal tissue and indicate that the alp ha(1)-adrenoceptor-induced contraction requires the opening of voltage -gated Ca2+ channels and the release of Ca2+ from intracellular stores .