Altered urinary sodium excretion response after central cholinergic and adrenergic stimulation of adult spontaneously hypertensive rats

Author(s)

Lutaif, Nelson A. ^[1] ; Gontijo, Livia M. ^[1] ; Figueiredo, Jose F. ^[1] ; Gontijo, Jose A. R. ^{[1, 2]}

Affiliation

^[1] Univ Estadual Campinas, Fac Ciencias Med, Nucleo Med & Cirurgia Expt, Lab Metab Hidrosalino, Disciplina Med Interna, BR-13083970 Campinas, SP - Brazil

^[2] Univ Estadual Campinas, Fac Ciencias Med, Dept Clin Med, BR-13083887 Campinas, SP - Brazil

• Document type: Journal article
• Source: Journal of Physiological Sciences; v. 65, n. 3, p. 265-275, MAY 2015.
• Web of Science Citations: 2

Abstract

In this study, we hypothesized that blunting of the natriuresis response to intracerebroventricularly (i.c.v.) microinjected cholinergic and adrenergic agonists is involved in the development of hypertension in spontaneously hypertensive rats (SHR). We evaluated the effect of i.c.v. injection of cholinergic and noradrenergic agonists, at increasing concentrations, and of muscarinic cholinergic and alpha 1 and alpha 2-adrenoceptor antagonists on blood pressure and urinary sodium handling in SHR, compared with age-matched Wistar Kyoto rats (WR). We confirmed that CCh and NE microinjected into the lateral ventricle (LV) of conscious rats leads to enhanced natriuresis. This response was associated with increased proximal and post-proximal sodium excretion accompanied by an unchanged rate of glomerular filtration. We showed that cholinergic-induced natriuresis in WR and SHR was attenuated by previous i.c.v. administration of atropine and was significantly lower in the hypertensive strain than in WR. In both groups the natriuretic effect of injection of noradrenaline into the LV was abolished by previous local injection of an alpha 1-adrenoceptor antagonist (prazosin). Conversely, LV alpha 2-adrenoceptor antagonist (yohimbine) administration potentiated the action of noradrenaline. The LV yohimbine pretreatment normalized urinary sodium excretion in SHR compared with age-matched WR. In conclusion, these are, as far as we are aware, the first results showing the importance of interaction of central cholinergic and/or noradrenergic receptors in the pathogenesis of spontaneous hypertension. These experiments also provide good evidence of the existence of a central adrenergic mechanism consisting of alpha 1 and alpha 2-adrenoceptors which works antagonistically on regulation of renal sodium excretion. (AU)