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

Abstract

Effects of arginine-vasopressin (AVP) on the cardiac L-type Ca²⁺ current (I_Ca,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 μmol/l) appeared to have little effect on I_Ca,L, but the same concentrations of AVP consistently increased I_Ca,L using the nystatin-perforated patch clamp mode. The stimulatory effect was blocked by either OPC-21268 (8 μmol/l), a selective V₁ receptor antagonist, or staurosporine (10 nmol/l), an inhibitor of protein kinases. AVP further increased the amplitude of I_Ca,L previously augmented maximally by isoprenaline (1 μmol/l). When myocytes were pretreated with ryanodine (2 μmol/l) or cyclopiazonic acid (3 μmol/l), the increase in I_Ca,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,L. The AVP-induced increase in I_Ca,L may require intracellular constituents, which might be washed out during the use of the conventional whole-cell patch clamp method.