Dopamine has been recognized as an important modulator of central as well as peripheral physiologic functions in both humans and animals.
Dopamine receptors have been identified in a number of organs and tissues, which include several regions within the central nervous system, sympathetic ganglia and postganglionic nerve terminals, various vascular beds, the heart, the gastrointestinal tract, and the kidney. The peripheral
dopamine receptors influence cardiovascular and renal function by decreasing afterload and vascular resistance and promoting
sodium excretion. Within the kidney,
dopamine receptors are present along the nephron, with highest density on proximal tubule epithelial cells. It has been reported that there is a defective
dopamine receptor, especially D(1) receptor function, in the proximal tubule of various animal models of
hypertension as well as in humans with
essential hypertension. Recent reports have revealed the site of and the molecular mechanisms responsible for the defect in D(1) receptors in
hypertension. Moreover, recent studies have also demonstrated that the disruption of various
dopamine receptor subtypes and their function produces
hypertension in rodents. In this review, we present evidence that
dopamine and
dopamine receptors play an important role in regulating renal
sodium excretion and that defective renal
dopamine production and/or
dopamine receptor function may contribute to the development of various forms of
hypertension.