Reflexes fail to reduce pressor activity of vasopressin in spontaneous hypertension

Abstract

Pressor responses and heart rate responses were recorded in spontaneously hypertensive rats (SHR) and in Wistar-Kyoto (WKY) rats during intravenous infusions of arginine vasopressin and phenylephrine under two experimental situations, first when cardiovascular reflexes were impaired by pretreatment with a ganglionic blocking agent (pentolinium) and second, when reflexes remained intact. In rats with ganglia blocked, pressor responses of SHR to vasopressin or to phenylephrine were similar to those of WKY rats. In rats with intact reflexes, pressor responses of SHR to phenylephrine were also similar to those of WKY rats but, in contrast, pressor responses of SHR to vasopressin were enhanced. Heart rate fell much more for any given elevation of blood pressure in WKY rats than in SHR during infusions of vasopressin and phenylephrine, and the bradycardia associated with these pressor agents was largely abolished by pentolinium. The results are consistent with the hypothesis that baroreflexes buffer the pressor activity of vasopressin in the normotensive WKY rat and that an impairment of baroreflex activity in SHR contributes to the enhanced pressor activity of vasopressin in these rats.

OPC-21268, a vasopressin V1 antagonist, produces hypotension in spontaneously hypertensive rats.

“…Despite an enhanced pressor response to AVP in SHR, heart rate fell much more for any given elevation of blood pressure in Wistar-Kyoto rats than SHR during infusion of AVP. 9 In the present study, heart rate did not change despite a considerable decrease in blood pressure (Fig 4). This result may suggest a dysfunction in the baroreceptor reflex.…”

α2-Adrenergic receptors in NTS facilitate baroreflex function in adult spontaneously hypertensive rats

“…In the spontaneously hypertensive rat (SHR), for example, resting blood pressure may be 40-60 mmHg higher than in normotensive rats, and the sigmoid curve describing baroreflex control of mean arterial pressure (MAP) and sympathetic nerve activity is shifted upward but remains parallel to the normal baroreflex curve (9,12,38). In contrast, baroreflex control of heart rate (HR) is markedly attenuated in the SHR (2,15,21,34), despite a resting HR that is comparable to that of its normotensive control, the Wistar-Kyoto rat (WKY). Because baroreflex impairment is present in many forms of hypertension and may contribute to the development and maintenance of the disease (9,10,15,31,34), an understanding of the neurochemical mechanisms involved is of great importance.…”

Role of Vasopressin and .ALPHA.1-Adrenergic Mechanism in the Cardiovascular Effects of Intracerebroventricular Administration of Somatostatin in Rats.

“…A possible pressor role of AVP has also been postulated in some hypertensive models (6,7). Intravenous administration of AVP has been shown to increase blood pressure (8)(9)(10). Several studies have indicated that central a-adrenergic mechanisms mediate the control of AVP secretion (11)(12)(13)(14)(15).…”