Central alpha-2 adrenergic mechanisms in the renal nerve mediated natriuresis and diuresis produced by acute volume expansion

Abstract

To determine whether central alpha-2 adrenergic mechanisms are involved in the renal nerve mediated natriuresis and diuresis produced by acute volume expansion, urine flow and sodium excretion from innervated and denervated kidneys were measured before and after acute volume expansion (1 ml/min for 20 min) in the presence or absence of intracerebroventricular yohimbine (8 μg/kg/min), an alpha-2-antagonist, in Inactin-anesthetized Sprague-Dawley rats. The innervated to denervated (I/D) ratio for urine flow and sodium excretion indicated that acute volume expansion caused a greater natriuresis and diuresis from the intact kidney compared to the denervated kidney. However, these I/D ratios during acute volume expansion were significantly reduced in the presence of yohimbine i.c.v. Furthermore, central administration of clonidine, an alpha-2 agonist, produces a renal nerve mediated natriuresis. These data suggest that central alpha-2 adrenergic mechanisms may be involved in producing the renal sympatho-inhibition, which subsequently produces natriuresis and diuresis, in response to acute volume expansion.