Dopamine receptors modulate sodium excretion in denervated kidney.

Abstract

Dopamine (DA) modulates sodium excretion by the innervated kidney. To examine the role of DA in the denervated (DNX) kidney the effects of the DA1/DA2 antagonist cis-flupenthixol (group 2, n = 7) (10 nmol X kg-1 X min-1), given intravenously in saline-loaded Wistar-Kyoto rats after acute unilateral left DNX, were compared with a placebo group (group 1, n = 7) and a group that received the DA1 antagonist SCH 23390 (group 3, n = 7) at 2.5 nmol X kg-1 X min-1. Pentobarbital sodium anesthesia was employed. Adequacy of DNX was assessed by a natriuresis and decrease in renal norepinephrine content in the DNX kidney and an antinatriuresis in the innervated right kidney. Mean arterial pressure slightly decreased in the placebo group (group 1, 106.7 +/- 2.2 vs. 99.3 +/- 2.4 mmHg) and after cis-flupenthixol (group 2, 108.8 +/- 2.7 vs. 92.8 +/- 1.8 mmHg) but not after SCH 23390 (group 3, 105.6 +/- 1.6 vs. 103 +/- 1.1 mmHg). Glomerular filtration rate was not affected by placebo or SCH 23390 in the DNX or innervated kidney but did slightly decrease after cis-flupenthixol in the DNX kidney. Sodium and water excretion after drug administration differed among the groups. In the DNX kidney urine flow decreased only in group 2, whereas fractional sodium excretion decreased modestly (P less than 0.05 paired t test) with SCH 23390 (3.53 +/- 0.34 vs. 2.89 +/- 0.20%) markedly with cis-flupenthixol (3.18 +/- 0.50 vs. 1.21 +/- 0.18%) and was unchanged in the placebo group (3.25 +/- 0.61 vs. 3.45 +/- 0.45%).(ABSTRACT TRUNCATED AT 250 WORDS)