Enhancement by arginine vasopressin of the L-type Ca2+ current in guinea pig ventricular myocytes

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