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D3 dopamine receptor (D3 R)–deficient mice have renin-dependent hypertension associated with sodium retention, but the hypertension is mild. To determine whether any compensatory mechanisms in the kidney are involved in the regulation of blood pressure with disruption ofDrd3 , we measured the renal protein expression of all dopamine receptor subtypes (D1 R, D2 R, D4 R, and D5 R) in D3 R homozygous (D3 −/− ) and heterozygous (D3 +/− ) knockout mice and their wild-type (D3 +/+ ) littermates. The renal immunohistochemistry and protein expression of D5 R were increased (n=5/group) in D3 −/− mice; renal D4 R protein expression was decreased, whereas renal protein expressions of D1 R and D2 R were similar in both groups. Renal D5 R protein expression was also increased in D3 +/− (n=5/group) relative to D3 +/+ mice, whereas D1 R, D2 R, and D4 R protein expressions were similar in D3 +/− and D3 +/+ mice. The increase in renal D5 R protein expression was abolished when D3 −/− mice were fed a high-salt diet. Treatment with the D1 -like receptor antagonist, SCH23390, increased the blood pressure in anesthetized D3 −/− but not D3 +/+ mice (n=4/group), suggesting that the renal upregulation of D5 R may have minimized the hypertension in D3 −/− mice. The renal D5 R protein upregulation was not caused by increased transcription because renal mRNA expression of D5 R was similar in D3 −/− and D3 +/+ mice. Our findings suggest that the renal upregulation of D5 R may have minimized the hypertension that developed in D3 −/− mice.

Upregulation of Renal D 5 Dopamine Receptor Ameliorates the Hypertension in D 3 Dopamine Receptor–Deficient Mice

Upregulation of Renal D ₅ Dopamine Receptor Ameliorates the Hypertension in D ₃ Dopamine Receptor–Deficient Mice