The clinical effects of DA, an endogenous nonselec-tive direct and indirect adrenergic and dopaminergic agonist, vary markedly with the dose. At low doses (0.5–3 mcg/kg/min), DA primarilyactivates dopaminergic receptors (specifically, DA1 receptors); stimulation of these receptors vasodilates the renal vasculature and promotes diuresis and natriuresis. Although this action increases renal blood flow, use of this “renal dose” does not impart any beneficial effect on renal function. When used in moderate doses (3–10 mcg/kg/min), β1-stimulation increases myocardial contractility, heart rate, sys-tolic blood pressure, and cardiac output. Myocardial oxygen demand typically increases more than sup-ply. The α1-effects become prominent at higher doses (10–20 mcg/kg/min), causing an increase in peripheral vascular resistance and a fall in renal blood flow. The indirect effects of DA are due to release of norepinephrine from presynaptic sympa-thetic nerve ganglion.
DA is commonly used in the treatment of shock to improve cardiac output, support blood pres-sure, and maintain renal function. It is often used in combination with a vasodilator (eg, nitroglycerinor nitroprusside), which reduces afterload and fur-ther improves cardiac output. The chronotropic and proarrhythmic effects of DA limit its usefulness in some patients.
DA is administered as a continuous infusion at a rate of 1–20 mcg/kg/min. It is most commonly sup-plied in 5–10 mL vials containing 200 or 400 mg of DA.