Endogenous Renal Dopamine and Control of Blood Pressure

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Abstract
Activation of specific receptors for dopamine in the renal vasculature and tubules leads to increases in glomerular filtration, and to diuresis and natriuresis. There is evidence for intrarenal production and release of dopamine, which may originate from two sources: tubular decarboxylation of plasma 1-DOPA and a population of dopaminergic sympathetic neurons that innervate the renal cortex. Studies of plasma and urinary catecholamine levels indicate that dopamine is released within the kidney in response to sodium loading and to activation of sensory pathways related to nociception and chemoreception. There is also evidence for deficient renal release of dopamine in patients with renovascular or essential hypertension. Collectively, the available data suggest that intrarenal dopamine has a physiological function in control of blood volume and blood pressure, and that defects in this control may be implicated in the aetiology of some hypertensive states.