Enhancement by Arginine Vasopressinof the L-Type Ca2+ Current in Guinea PigVentricular Myocytes

Effects of arginine-vasopressin (AVP) on the cardiac L-type Ca2+ current (ICa,L) were investigated in single ventricular cells of guinea pig hearts by the conventional and nystatin-perforated patch clamp methods. Using the conventional whole-cell clamp method, AVP (0.01-1 micromol/l) appeared to have little effect on ICa,L, but the same concentrations of AVP consistently increased ICa,L using the nystatin-perforated patch clamp mode. The stimulatory effect was blocked by either OPC-21268 (8 micromol/l), a selective V1 receptor antagonist, or staurosporine (10 nmol/l), an inhibitor of protein kinases. AVP further increased the amplitude of ICa,L previously augmented maximally by isoprenaline (1 micromol/l). When myocytes were pretreated with ryanodine (2 micromol/l) or cyclopiazonic acid (3 micromol/l), the increase in ICa,L by AVP was partially reduced. The present results indicate that protein kinase C might be involved in the AVP-induced increase of ICa,L. The AVP-induced increase in ICa,L may require intracellular constituents, which might be washed out during the use of the conventional whole-cell patch clamp method.