Impaired dipsogenic and renal response to repetitive intracerebroventricular angiotensin II (AngII) injections in rats

Abstract

The role of the central nervous system (CNS) in the control of blood pressure and hydrosaline homeostasis has been demonstrated by several studies. While circulating angiotensin II (AngII) tends to retain sodium by a direct renal action as well as through aldosterone release, stimulation of brain AngII receptors has been reported to induce natriuresis. Repetitive intracerebroventricular AngII injection was recently demonstrated to be capable of leading to desensitisation of the dipsogenic effect of AngII stimuli. The aim of the current study was to investigate a possible central desensitisation to AngII stimuli by observing the effects of a low-concentration solution of AngII on the dipsogenic and natriuretic mechanisms in conscious rats, compared with appropriate age-matched 0.15 M NaCl-injected subjects, as evaluated by lithium clearance. The present report confirmed earlier reports on the potent natriuretic and dipsogenic effects of central AngII receptor stimulation. Natriuresis is mediated by a decrease in sodium reabsorption in the proximal and post-proximal tubule segments of the nephron. The current findings lend further support to the idea that AngII, in the CNS, is instrumental in the regulation of body fluid homeostasis. The magnitude of the dipsogenic and renal response to AngII was significantly decreased by repetitive stimulus.

Early changes of hypothalamic angiotensin II receptors expression in gestational protein-restricted offspring: effect on water intake, blood pressure and renal sodium handling

“…22 The current study also confirmed that AngII, when microinjected into the lateral ventricle of conscious NP rats, produced a marked dipsogenic effect. 14,15 Additionally, for the first time, we demonstrate that the dipsogenic effect of i.c.v. 4 nmol AngII was significantly lower in the LP offspring than in NP rats.…”

“…dose-response AngII (at 40 pmol to 40 nmol) injection: rats received 2 µl AngII and the volume of water consumed was measured during the next 30 min. 14,15 …”

“…A 23-gauge guide stainless steel cannula with an indwelling 30-gauge obturator was stereotaxically implanted into the lateral cerebral ventricle (LCV) using previously reported techniques and pre-established coordinates: anteroposterior, 0.2 mm from bregma, lateral 1.5 mm and vertical -2.8 mm. 14,15 Rats were allowed a one-week recovery before testing for cannula patency and position. Cannulas were considered patent and correctly positioned by Evans blue infusion through the i.c.v.…”

“…10 Cell bodies at the subfornical organ (SFO), hypothalamic paraventricular nucleus (PVN), medial preoptic lateral nucleus (MnPO) and organum vasculosum of the lamina terminalis (OVLT) express high levels of AT 1 R, which respond rapidly to an AngII stimulus. 11 Most studies conclude that centrally administered AngII induces thirst by activating AT 1 R in neurons of the lamina terminalis area, [12][13][14][15] whereas in the IUGR models that relationship has not yet been investigated. Also, the action of AT2 R in CNS function is not well known.…”

Impact of taurine supplementation on blood pressure in gestational protein-restricted offspring: Effect on the medial solitary tract nucleus cell numbers, angiotensin receptors, and renal sodium handling

“…33,34 A previous study reported that, in conscious rats, central AngII induces an immediate reduction in the efferent renal nerve and enhanced renin-angiotensin dipsogenic and natriuretic response. 17,35,36 Otherwise, further studies are needed to evaluate the repercussion of taurine supplementation directly on kidney morphology and development, and vascular reactivity.…”