Effects of arginine-vasopressin (AVP) on the cardiac L-type Ca<sup>2+</sup> current (I<sub>Ca,L</sub>) 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<sub>Ca,L</sub>, but the same concentrations of AVP consistently increased I<sub>Ca,L</sub> using the nystatin-perforated patch clamp mode. The stimulatory effect was blocked by either OPC-21268 (8 μmol/l), a selective V<sub>1</sub> receptor antagonist, or staurosporine (10 nmol/l), an inhibitor of protein kinases. AVP further increased the amplitude of I<sub>Ca,L</sub> 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<sub>Ca,L</sub> by AVP was partially reduced. The present results indicate that protein kinase C might be involved in the AVP-induced increase of I<sub>Ca,L</sub>. The AVP-induced increase in I<sub>Ca,L</sub> may require intracellular constituents, which might be washed out during the use of the conventional whole-cell patch clamp method.

Kurata, S., Ishikawa, K., & Iijima, T. (1999). Enhancement by Arginine Vasopressinof the L-Type Ca²⁺ Current in Guinea PigVentricular Myocytes. Pharmacology, 59(1), 21–33. Portico.