Dopamine reacts with blood vessel receptors, causing both dilatation and constriction. In the dog the vasodilator receptors are presentin the renal and mesenteric vascular beds but absent from the vascular beds of the limb. The vasoconstrictor receptors, alpha adrenergic in type, are present in both somatic and visceral regions. The net effect of intravenously administered dopamine on regional flows will depend on the relative intensity of these opposing effects and on changes in blood pressure. The present study was an attempt to evaluate the significance of the vasoconstrictor action of dopamine infused at nonpressor doses, i.e., 3 to 6 µg/kg/min. Renal and femoral blood flows were measured simultaneously, and systemic hemodynamics were evaluated before and after administration of the alpha adrenergic antagonists, phentolamine and phenoxybenzamine.
The results indicate that the vasoconstrictor property of dopamine is masking a mild depressor effect, ranging in magnitude from 10 to 25 mm Hg. Dopamine increases cardiac output independently of its alpha adrenergic properties. Dopamine causes an increase in renal blood flow of equal magnitude before and after alpha adrenergic block but reduces renal vascular resistance to a lower level after alpha block, reflecting the depression in blood pressure. Dopamine does not alter femoral vascular resistance either before or after alpha adrenergic block. However, femoral blood flow is decreased by dopamine after alpha block, secondary to the depression of blood pressure. It is concluded that under the conditions of these studies, alpha adrenergic block enhances the vasodepressor property of dopamine and does not appreciably modify its ability to increase cardiac output and redistribute peripheral blood flow.
- © 1966 American Heart Association, Inc.