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What we can learn from the selective manipulation of dopaminergic receptors about the pathogenesis and treatment of hypertension?

The natriuretic response that accompanies an acute or a chronic sodium load results, in a large part, from dopamine produced by the renal proximal tubules. This paracrine/ autocrine effect of dopamine, mediated by occupancy of renal tubular dopamine D1 receptors, is impaired in spontaneous hypertension. Disruption of the D1A receptor gene in mice increases blood pressure. The D3 receptor is also present in renal proximal tubules and juxtaglomerular cells, and it may be an inhibitor of renin release. Disruption of the D3 receptor gene in mice also increases blood pressure, but the ability to excrete a sodium chloride load is not impaired. Thus, selective manipulation of dopamine receptor subtypes might aid in studies of the pathogenesis of essential hypertension and the design of novel drugs to treat high blood pressure.