The general goal of the studies described in this proposal is to understand the role of vasopressin in hypertension and the normal regulation of blood pressure. Specifically, these studies will examine the role of vasopressin in the hypertension that results from bilateral destruction of the area of the Al noradrenergic cells in the caudal ventrolateral medulla oblongata (the Al area). Preliminary data indicate that this model of hypertension, in both rabbit and rat, is dependent upon elevated levels of vasopressin in the blood produced by such lesions. The studies described in this proposal are designed to fully examine the role of vasopressin in this form of hypertension in rat. These studies will also examine the effects of lesions of the AL area in other pressor systems) i.e., sympatho-adrenal system and renin-agoiotension system), with the aim of determining how these systems interact with vasopressin to produce the fulminating hypertension caused by these lesions. The studies will involve pharmacologic manipulation of the vasopressin, sympathoadrenal, and renin-angiotension systems as will as assessing the roles of these systems be measuring indices of their activity (i.e., plasma vasopressin levels, plasma catecholamine levels, plasma renin activity). The preliminary observations (a) that infusions of vasopressin to levels similar to those produced by lesions of thr Al area do not elevate blood pressure and (b) that the rise in plasma vasopressin levels can be dissociated from changes in blood pressure by selective pharmacologic manipulation of the Al area will be further examined.. Thses studies should provide new and important information on the role of vasopressin in hypertension, and may therefore suggest new strategies for the effective control of blood pressure in hypertension patients.
| Catelli, J M; Sved, A F (1988) Lesions of the AV3V region attenuate sympathetic activation but not the hypertension elicited by destruction of the nucleus tractus solitarius. Brain Res 439:330-6 |
| Catelli, J M; Giakas, W J; Sved, A F (1987) GABAergic mechanisms in nucleus tractus solitarius alter blood pressure and vasopressin release. Brain Res 403:279-89 |
| Sved, A F; Felsten, G (1987) Stimulation of the locus coeruleus decreases arterial pressure. Brain Res 414:119-32 |
| Sved, A F (1986) Peripheral pressor systems in hypertension caused by nucleus tractus solitarius lesions. Hypertension 8:742-7 |
| Sved, A F (1986) Pontine pressor sites which release vasopressin. Brain Res 369:143-50 |
| Sved, A F; Scott, P J; Kole, M (1985) Cerebellar lesions attenuate vasopressin release in response to hemorrhage. Neurosci Lett 55:65-70 |
| Sved, A F (1985) Clonidine can lower blood pressure by inhibiting vasopressin release. Eur J Pharmacol 109:111-6 |
