Urinary dopamine and renal handling of L-DOPA in fasted spontaneously hypertensive rats.

A defective renal dopaminergic system has been suggested to contribute, via impaired sodium excretion, to the pathogenesis of hypertension. Data according renal dopamine (DA) release in hypertension, however, are inconsistent. In the present study, we compared urinary DA excretion (UDAV), plasma free DA (PDA), and renal tissue DA contents (TDA) of young spontaneously hypertensive rats (SHR), Wistar-Kyoto (WKY), and Sprague-Dawley (SD) rats. Since the protein intake dominantly controls UDAV, fasted animals were used to exclude the influence of feeding. Conscious WKY and SHR had a similar UDAV which was lower compared to SD rats. Thiopental anesthesia increased UDAV in SHR and WKY but not in SD rats. TDA was higher in SHR compared to SD and WKY rats. To investigate the tubular capacity to generate DA, the response to L-DOPA infusion was assessed in two doses. 1 nmol/min/100 g body weight L-DOPA increased UDAV approximately 30-fold in all strains but did not affect tubular sodium excretion or renal hemodynamics. In contrast, infusion of 3 micromol/min/100 g body weight L-DOPA increased UDAV by five orders of magnitude and induced natriuresis, diuresis, and tachycardia. These effects were assigned to an increase in PDA and no significant differences were observed among the strains. We conclude that, regarding renal DA, (1) the differences among SHR, WKY, and SD rats rather appear to be strain related than hypertension associated; (2) the renal capacity of DA generation from L-DOPA is not impaired in SHR; (3) tubular DA at physiological concentrations does not alter sodium excretion significantly in normo- or hypertensive rats, and (4) the influence of anesthesia on UDAV should be considered in comparative studies.