To determine whether renal nerves are involved in natriuresis or diuresis produced by the intracerebroventricular administration of clonidine (0.2, 2.0, and 8 μg/kg/min, and 2.0 μl/min), urine flow, and sodium excretion were measured before and during clonidine administration from innervated and contralateral denervated kidneys in anesthetized (Inactin, 0.1 g/kg, ip) Sprague-Dawley rats. Baseline urine flow and sodium excretion were elevated after renal denervation prior to infusion of clonidine. Examining urine flow and sodium excretion before and during clonidine infusion indicated significant increases in urine flow and sodium excretion from the innervated kidneys but not from the denervated kidneys, possibly due to the renal sympatho-inhibition in the innervated kidney. However, the higher doses of clonidine (2 and 8 μg/kg/min) may have diffused out of the intracerebroventricular space into the peripheral circulation and produced their effect by a direct action on the kidney. Subsequently, two experiments were performed to distinguish between a central action and peripheral action. First, clonidine was administered centrally with concurrent administration of an α2-blocker, yohimbine (8 μg/kg/min, iv), peripherally. In a second experiment the dose of clonidine was reduced 10-fold such that this reduced dose did not produce a peripheral action but still produced the renal responses to central administration. The results of the latter two studies further confirmed that natriuresis and diuresis produced by intracerebroventricular administration of clonidine is in part mediated by renal nerves.
|Original language||English (US)|
|Number of pages||7|
|Journal||Proceedings of the Society for Experimental Biology and Medicine|
|State||Published - Jan 1993|
ASJC Scopus subject areas
- Biochemistry, Genetics and Molecular Biology(all)