All of the components of a complete dopamine system are present within the kidney, where dopamine acts as a paracrine substance in the control of sodium excretion. Dopamine receptors can be divided into D₁-like (D₁ and D₅) receptors that stimulate adenylyl cyclase and D₂-like (D₂, D₃, and D₄) receptors that inhibit adenylyl cyclase. All 5 receptor subtypes are expressed in the kidney, albeit in low copy. Dopamine is synthesized extraneuronally in proximal tubule cells, exported from these cells largely into the tubule lumen, and interacts with D₁-like receptors to inhibit the Na⁺-H⁺ exchanger and Na⁺,K⁺-ATPase, decreasing tubule sodium reabsorption. During moderate sodium surfeit, dopamine tone at D₁-like receptors accounts for ≈50% of sodium excretion. In experimental and human hypertension, 2 renal dopaminergic defects have been described: (1) decreased renal generation of dopamine and (2) a D₁ receptor-G protein coupling defect. Both defects lead to renal sodium retention, and each may play an important role in the pathophysiology of essential hypertension.