Effects of Prazosin on Coronary and Left Ventricular Dynamics in Conscious Dogs

The left ventricular (LV) and coronary vascular effects of prazosin, a drug that reduces peripheral vascular resistance by blocking postsynaptic a receptors, were examined in conscious dogs. Prazosin, 0.07 mg/kg/mmn i.v. for 7 minutes, induced sustained hypotensive effects for more than 12 hours. The peak effects occurred 3045 minutes after administration. Prazosin increased heart rate by 28 ± 9%, did not change mean coronary blood flow significantly, decreased mean arterial pressure by 15 i 4%, LV enddiastolic diameter by 10 + 2%, LV end-systolic diameter by 8 ± 2%, late diastolic coronary resistance by 22:7%, and—LV dP/dt by 9 i 4%. These effects of prazosin were not altered substantially by maintaining heart rate constant with electrical pacing or by pretreatment with, B-adrenergic blockade. However, after chronic reserpine treatment, prazosin did not reduce either mean arterial pressure or late diastolic coronary resistance. The a-blocking properties of the drug were established when prazosin attenuated pressor responses to phenylephrine, norepiphrhrine and bilateral carotid occlusion. Thus, in conscious dogs with heart rate constant, prazosin, by blocking a-adrenergic receptors, induces prolonged coronary vasodilation associated with reductions in the major determinants of myocardial oxygen consumption, e.g., arterial and LV pressures, LV end-diastolic diameter and LV dP/dt. However, the coronary vasodilation was not intense enough to increase coronary blood flow above control levels.