Role of dopamine in congestive heart failure: a contemporary appraisal

The pharmacodynamic effects of dopamine, an endogenous catecholamine, are complex and mediated through selective activation of specific dopaminergic and adrenergic receptors in a dose dependent manner. Low dose dopamine (0.5-2 micro g/kg/min) induces intrarenal vasodilatation, augmented renal blood flow, and inhibition of renal tubular sodium reabsorption through direct stimulation of peripheral dopaminergic receptors DA1 and DA2. Intermediate doses (3-10 micro g/kg/min) favor beta(1)-adrenergic receptor stimulation of the heart and peripheral vasoconstriction due to alpha-adrenergic receptor stimulation. At higher does (>10 micro g/kg/min), an elevated systemic vascular resistance prevails and the salutary effect on renal blood flow is diminished or lost. Dopamine is no longer favored as a first line agent for use in congestive heart failure (CHF) owing to the superior pharmacodynamic properties of dobutamine and is more properly used as an agent for vasopressor therapy. Studies have not supported the renal sparing effect of low dose dopamine for critically ill patients with incipient or established acute renal failure due to ischemia or nephrotoxicity. Evidence that low dose dopamine protects renal function during vigorous diuresis for CHF associated with renal insufficiency has clinical support and a rationale for its use. (c)1999 by CHF, Inc.