1. The present investigation was carried out to elucidate the possible role of the renin-angiotensin system in modulating coronary vasomotor responses in eight patients with uncomplicated mild essential hypertension with no electrocardiographic-echocardiographic evidence of left ventricular hypertrophy.
2. Systemic and coronary haemodynamics were monitored at baseline and during intravenous infusion of angiotensin II at a subpressor dose (3 ng min−1 kg−1 for 15 min) and at a pressor dose (13 ng min−1 kg−1 for 15 min) both at rest and during handgrip exercise. Infusion of the subpressor dose of angiotensin II decreased coronary sinus blood flow at rest (207 ± 10 versus 182 ± 9 ml/min, P < 0.05) without a significant change in mean arterial pressure, heart rate or mean right atrial pressure. The performance of handgrip at baseline and during infusion of the subpressor dose of angiotensin II resulted in 55% (321 ± 13 versus 207 ± 10 ml/min) and 44% (263 ± 16 versus 182 ± 9 ml/min) increases in coronary sinus blood flow, respectively, in response to comparable increments in the rate-pressure product. At rest, infusion of the pressor dose of angiotensin II increased both coronary sinus blood flow (235 ± 11 versus 207 ± 10 ml/min, P<0.01) and the rate-pressure product (134 ± 5 versus 111 ± 8 mmHg beats/min, P<0.01). The increase in coronary sinus blood flow during isometric exercise was less than control (309 ± 18 versus 321 ± 13 ml/min, P<0.01).
3. It is thus concluded that (1) the opposite effects of angiotensin II on coronary blood flow are dose-dependent, and that (2) angiotensin II competes with the ability of the coronary arteries to dilate during handgrip exercise.