Role of anteroventral third ventricle and vasopressin in renal response to stress in borderline hypertensive rats.

Abstract

The borderline hypertensive rat is the first filial offspring of the spontaneously hypertensive rat and the Wistar-Kyoto rat In response to acute environmental stress (air jet), the borderline hypertensive rat exhibits a diuretic response, whereas the parental strains exhibit an antidiuretic response (spontaneously hypertensive rat) or no change in urine flow rate (Wistar-Kyoto rat). This study sought to investigate the role of the periventricular tissue surrounding the anteroventral third ventricle and vasopressin release in the diuretic response of the borderline hypertensive rat to acute environmental stress. Sixteen-week-old borderline hypertensive rats who had consumed a 1% NaCl diet for 10-12 weeks were given either electrolytic lesions of the anteroventral portion of the third ventricle or sham lesions. When exposed to acute environmental stress 4 weeks later, the increase in volume of dilute urine seen in the sham-lesion rats was not observed in the lesion rats. Plasma vasopressin concentration was decreased by acute environmental stress in the sham-lesion rats (15.2±4.0 to 10.9±1.7 pg/ml, p<0.05) but was unchanged in the lesion rats (12J±2.0 to 13.4±4.0 pg/ml). In a separate group of intact borderline hypertensive rats, a constant intravenous infusion of vasopressin prevented the diuretic response to acute environmental stress. The results suggest that acute environmental stress produces a diuresis in the borderline hypertensive rats via a decrease in plasma vasopressin concentration that is dependent on the integrity of the periventricular tissue of the anteroventral portion of the third ventricle. (Hypertension 1991;17:755-762) T he borderline hypertensive rat (BHR) is a genetic model of environmentally induced hypertension. The BHR is the first filial offspring of the spontaneously hypertensive rat (SHR) and the normotensive Wistar-Kyoto (WKY) rat and possesses genetic information from both parents. As described by Lawler and colleagues, the BHR become permanently hypertensive when subjected to a timelimited period of exposure to environmental stress 1 " 3 or to increased dietary sodium chloride intake.

Autonomic mechanisms underpinning the stress response in borderline hypertensive rats

“…Enhanced sympathoadrenal response (Sanders et al 1988; Sanders & Lawler, 1992; Fuchs et al 1998), sensitization of sympathetic response (Mansi & Drolet, 1997), salt‐dependent enhancement of sympathetic to vascular signalling (Brown et al 1999), as well as decreased vascular endothelium‐dependent relaxation (Fuchs et al 1998; Giulumian et al 1999; Bernatova & Csizmadiova, 2006) were mentioned as peripheral mechanisms. Central α 2 ‐adrenergic receptors (Di Bona & Jones, 1991 b ) and the anteroventral third ventricle region (Hatton et al 1991) were suggested as the source of increased central sympathetic drive that underlies cardiovascular hyper‐responsiveness to environmental challenges (Di Bona & Jones, 1991 a ; Sanders & Lawler, 1992). However, others failed to record enhanced sympathoadrenal and catecholamine responsiveness to environmental challenges in the BHR (Kirby et al 1989; Stratton et al 1994), so the mechanisms that underlie cardiovascular hyper‐responsiveness of BHRs to environmental challenges still remain controversial.…”

Effects of Novelty Stress on Vasopressin and Oxytocin Secretion by the Pituitary in the Rat

“…Associatively or non-associatively applied fear-related emotional stress has been shown to suppress vasopressin secretion in rats (8-1 1). Emotional stress such as isolation stress (12), air jet stress applied to the head (13) or repeated chronic restraint of body movements (14) has been also shown to induce the suppressive vasopressin response. The present results suggest that novelty stress suppresses vasopressin secretion.…”