Effects of a calcium-channel antagonist on large and small coronary arteries in conscious dogs.

Abstract

The effects of i.v. nifedipine, 20 micrograms/kg, on left ventricular (LV) pressure, dP/dt, aortic pressure, heart rate, LV diameters, cardiac output, coronary blood flow and left circumflex coronary arterial diameter, and calculations of late diastolic coronary and total peripheral resistances and left circumflex coronary cross-sectional area were examined in 11 conscious dogs. In dogs with spontaneous rhythm, nifedipine induced an early, transient response characterized by hypotension and peak increases in coronary blood flow and decreases in total peripheral and late diastolic coronary vascular resistances. The peak effects on large coronary arteries were observed 2--5 minutes later, when mean arterial pressure was only 8.2 +/- 1.6 mm Hg below control and LV end-diastolic pressure and diameter were not significantly different from control. LV dP/dt was elevated by 7.1 +/- 1.1%, heart rate was elevated by 25 +/- 3.3 beats/min, and cardiac output remained elevated by 54 +/- 7.4%. At this time, coronary cross-sectional area was elevated by 26 +/- 3.0%, late diastolic coronary vascular resistance was reduced by 50 +/- 2.7%, and total peripheral resistance was 40 +/- 3.8% below control. The coronary sinus oxygen content was elevated by 3.4 +/- 0.8 vol% and the arteriovenous oxygen difference fell by 3.5 +/- 0.8 vol%. After beta-adrenergic blockade with propranolol and with heart rate constant or varying, the increases in coronary cross-sectional area and decreases in late diastolic coronary vascular resistance induced by nifedipine were still observed, but were significantly smaller (p less than 0.01). Thus, nifedipine dilates both large coronary arteries and coronary resistance vessels, effects that could be attributed in part to beta-adrenergic mechanisms. Nifedipine also exerts potent effects on coronary and peripheral arterial vessels, but has little effect on preload.