RENAL NERVES AND D-1-DOPAMINE RECEPTOR-MEDIATED NATRIURESIS

The resistance of the spontaneously hypertensive rat (SHR) kidney to t he natriuretic effect of dopamine and D-1 agonists may be due to incre ased renal nerve activity. Therefore, we compared the effects of the i ntrarenal arterial infusion of the D-1 agonist, SKF 38383, into the de nervated (DNX) kidney of saline-loaded-anesthetized SHR and its contro l, the Wistar-Kyoto (WKY) rat. In both WKY and SHR, DNX of the left ki dney slightly decreased urine flow (UV) and absolute (UNaV) and fracti onal sodium excretion (FENa) in the innervated right kidney;neither ve hicle nor D-1 agonist infusion exerted any effect. In the left kidney, denervation increased UV, UNaV, and FENa to a similar degree in WKY a nd SHR (2-fold), without affecting: renal blood flow, glomerular filtr ation rate, or blood pressure. In WKY but not in SHR after DNX, the D- 1 agonist dose-dependently increased UV, UNaV, and FENa in the denerva ted kidney. We conclude that the decreased natriuretic effect of D-1 a gonists in the SHR is not due to increased renal nerve activity. These data support our previous studies implicating a defect of the D-1 rec eptor or its regulation in the kidney in genetic hypertension.