Effect of membrane potential on H1-receptor-mediated 45Ca influx in coronary artery

These studies were undertaken to determine whether agonist-induced 45Ca influx in the coronary artery is modified under conditions in which Na+ pump activity (and consequently membrane potential) is altered. 45Ca influx and contraction were measured in the rabbit coronary artery with the H1-receptor agonist 2-(2-aminoethyl)pyridine (AEP, 10(-4) M) after prolonged Na+ pump block (leading to profound depolarization) and after enhanced Na+ pump activity (leading to hyperpolarization). AEP contracted vessels, enhanced 45Ca influx into the smooth muscle, and increased 45Ca efflux. The AEP-induced contraction was reduced but not abolished with either nifedipine (10(-6) M) or Ca(2+)-free solution. In tissues subjected to prolonged Na+ pump block AEP caused contraction but 45Ca influx was not increased over the unstimulated tissue. Ca(2+)-free solution and nifedipine reduced but did not abolish these contractions. In tissues with enhanced Na+ pump activity AEP caused contraction but 45Ca influx was not increased. Ca(2+)-free solution reduced these contractions but nifedipine did not. We conclude that the measurable 45Ca influx changes in a manner that is compatible with the characteristics of voltage-gated Ca2+ channels that have a low open probability during hyperpolarization and are inactivated by a period of long slow depolarization.