Interaction between calcium and hydrogen ions in canine coronary arteries.

In vitro experiments were carried out to study the effects of "respiratory" and "metabolic" acid-base alterations on canine coronary arteries precontracted by high potassium. Alkalosis (pH 7.70 +/- 0.02) increased the coronary tone by 33 +/- 3% (P less than 0.05) and acidosis (pH 7.10 +/- 0.01) decreased it by 30 +/- 3% (P less than 0.05). The tension stabilized in approximately 15 mins and its variation was of similar extent whether changes in extracellular pH were produced by changes in PCO2 or in bicarbonate concentration. The contractile changes were not abolished neither by alpha or beta adrenergic blockade nor by endothelium denudation. The effect of pH could not be offset by altering extracellular potassium or calcium when the plateau of the relationship between contractility of the smooth muscle and concentration of these ions was reached. When tonus developed by the strips and [Ca2+]0 were plotted reciprocally, DTmax significantly increased in alkalosis and decreased in acidosis. No significant changes in Ca50 ([Ca2+]0 necessary to obtain 50% of maximal force) were detected. pH changes did not modify Ca2+ influx but a relaxation of similar extent induced by nifedipine produced a detectable decrease in Ca2+ influx. Ca2+ efflux was augmented in acidosis and depressed in alkalosis. Our data do not support the hypothesis of hydrogen ion changes inducing calcium influx alterations in a competitive fashion as the mechanism involved to contract or relax conduit coronary arteries. On the contrary, they suggest that acid-base variations alter the contractile activity of vascular smooth muscle by modulating Ca2+ efflux.