Relative contributions of arginine vasopressin and angiotensin II to maintenance of systemic arterial pressure in the anesthetized water-deprived rat.

Abstract

We used a structural analogue of arginine vasopressin (AVP) and investigated the role of AVP in the maintenance of mean arterial pressure (AP) in anesthetized, water-deprived rats. The administration of [1(beta-mercapto-beta,beta-cyclopentamethylene propionic acid) 4-valine-8-D-arginine] vasopressin, d(CH2)5VDAVP, completely inhibited to 30-40 mma Hg rise in AP which normally accompanied the administration of 50 mU exogenous AVP (group 1). Thus, d(CH2)5VDAVP is a specific antagonist of the vascular effects of AVP. d(CH2)5VDAVP failed to significantly alter AP in water diuretic rats (group 3) and was without effect on urine osmolality during water diuresis or antidiuresis. However, bolus injection of d(CH2)5VDAVP into water deprived rats (group 2) prompted an abrupt fall in AP from 112 +/- 4 to 94 +/- 4 mm Hg (P less than 0.001). This fall in AP was transient, with return of AP to 110 +/- 4 mm Hg within 15 minutes. Administration of saralasin, an angiotensin II antagonist, not only prevented the compensation in AP, but also significantly magnified the maximal hypotensive response seen following d(CH2)5VDAVP (group 4). Discontinuing the saralasin allowed AP to return to baseline. Bilateral nephrectomy (group 5) also prevented the return of AP, further implicating endogenous angiotensin II as the specific mediator of the compensation in AP following d(CH2)5VDAVP administration. These studies clearly demonstrate that circulating AVP contributes to the maintenance of AP during water deprivation in the anesthetized rat. When this vascular action of AVP is blocked, angiotensin II assumes major responsibility for blood pressure regulation in the antidiuretic state.

Neonatal capsaicin treatment impairs vasopressin‐mediated blood pressure recovery following acute hypotension

“…Present evidence indicates that the reninangiotensin system, sympathetic nervous system and vasopressin may all interact and contribute to the maintenance of arterial blood pressure in normal (Gavras et al, 1982) and water-deprived states (Andrews & Brenner, 1981). We therefore used an angiotensin-converting enzyme inhibitor (captopril) and a ganglion blocker (pentolinium) to achieve an acute hypotension in which a possible influence of vasopressin on blood pressure could be discerned.…”

Conditions for secretion of vasopressin in pressor amounts in water-replete rats.

“…In the rat, secretion of vasopressin in pressor amounts has been observed following water-deprivation or hemorrhage (LAYCOCK et al, 1979;AISENBREY et al, 1981;ANDREWS and BRENNER, 1981;AL-AZZAWI and SHIRLEY, 1982). In water-replete and normovolemic rats, pressor amounts of vasopressin seem to be secreted only under restricted conditions.…”

Role of the Renal Nerve in Glucocorticoid Hypertension.

“…In our experiment too, dexamethasone treatment resulted in almost doubling of the urine volume, signiand hematocrit, and a marked decrease in body weight, indicating that treatment with an excess amount of dexamethasone caused volume depletion in these rats. The volume depletion should facilitate the activation of the renin-angiotensin system and the sympathetic nerve system through the baroreflex (Aisenbrey et al, 1981;Andrews and Brenner, 1981;Burnier et al, 1983 …”