Pharmacology: Dopamine is an endogenous catecholamine that is the immediate precursor of norepinephrine and stimulates adrenergic receptors of the sympathetic nervous system.
The drug has principally a direct stimulatory effect on 1-adrenergic receptors, but also appears to have an indirect effect by releasing norepinephrine from its storage sites. Dopamine also appears to act on specific dopaminergic receptors in the renal, mesenteric, coronary, and intracerebral vascular beds to cause vasodilation. This drug has little or no effect on 2-adrenergic receptors. In IV doses of 0.5-2 µg/Kg per minute, the drug acts predominantly on dopaminergic receptors: in IV doses of 2-10 µg/Kg per minute. the drug also stimulates 1-adrenergic receptors. In higher therapeutic doses, α-adrenergic, 1-adrenergic and dopaminergic stimulation. In low doses, cardiac stimulation and renal vascular dilation occur and in larger does vasoconstirction occurs. The 1-adrenergic effects of dopamine exert a positive inotropic effect on the myocardiurn and result in an increase in cardiac output because of increased myocardial contractility and stroke volume in healthy individuals and in patients with shock or congestive heart failure. Systolic blood pressure and pulse pressure may be increased as a result of increased cardiac output; however, peripheral vasodilation and the resulting decrease in peripheral resistance may counteract these effects. Blood pressure, therefore, may remain unchanged or be only slightly elevated. Heart rate is usually not substantially changed. In low to moderate doses, dopamine causes renal vasodilation, which results in increased renal blood flow and glomeruular filtration rate. Urine flow is variable affected, but usually increases. In high doses, α-adrenergic effects become more prominent and may result in increase of peripheral resistance and renal vasoconstriction. Blood pressure may return to normal if hypotension initially existed and may increase to hypertensive levels with excessive doses.