Vasopressin Release Induced by Water Deprivation: Effects of Centrally Administered Saralasin

Abstract

Uncertainty exists as to whether endogenous angiotensin activates brain mechanisms controlling vasopressin (AVP) secretion during dehydration. We injected various doses of saralasin into a lateral cerebroventricle (IVT) of conscious, male rats deprived of water for 48 h and killed them at different times. The concentration of AVP in the plasma (p[AVP]), measured by radioimmunoassay, was unaffected by saralasin. IVT pretreatment with 1-Sar-8-Ile-angiotensin II blocked maximal AVP release by IVT angiotensin, but this pretreatment did not reduce p[AVP] after 24, 48 or 72 h water deprivation. A 3-hour continuous IVT infusion of CSF or saralasin (10 μg/h) into 48-hour water-deprived rats revealed equivalent p[AVP] and urine volumes. When the infusions were continued for 3 h more with water available, control and saralasin-treated rats: (a) drank at similar rates, (b) excreted similar amounts of urine, and (c) reduced their p[AVP] levels to the same extent. IVT saralasin did not affect p[AVP] of rats dehydrated with hypertonic NaCl. Combined IVT saralasin and atropine reduced p[AVP] of 48-hour water deprived rats about 30% (p < 0.05). We conclude that redundancy exists for sensing, integrating and releasing vasopressin in dehydrated rats.

Role of the renin-angiotensin system in the control of vasopressin secretion in conscious dogs.

“…In previous studies, this approach has provided evidence that All is involved in the release of vasopressin that follows injection of isoproterenol and furosemide, two agents which increase renin secretion (Ramsay et al, 1978b;Siegel et al, 1979;Knepel and Meyer, 1980). In addition, it has been suggested that All may contribute to the elevated vasopressin levels in dehydrated rats (Yamaguchi et al, 1980(Yamaguchi et al, , 1982Keil et al, 1983). How-830 ever, All has not been implicated in the increase in vasopressin levels provoked by hemorrhage Share, 1972, 1973).…”

Role of Intracerebral Angiotensin Receptors in the Regulation of Vasopressin Release and the Cardiovascular System

“…Indeed, Hoffman et al [4] have recently reported that captopril given intracerebroventricularly was without effect on ADH release in duced by osmotic stimulation in anesthetized dogs. Sim ilarly, Keil et al [5] have observed that ADH release nor mally occurs in the presence of Ang II antagonist given intracerebroventricularly in rats dehydrated with hyper tonic N'aCl, and the drug per se does not affect the basal release of ADH.…”

“…1985 cularly has been shown to block ADH release in response to peripherally administered hypertonic saline [17] and to delay the onset of the dipsogenic reaction in rats [9]. How ever, it has also been reported that captopril, an Ang I con verting enzyme inhibitor, or saralasin given intracerebro ventricularly have no effects either on hypertonic saline in duced ADH release [4,5] or on the dipsogenic response [8]. Therefore, it is still controversial whether angiotensin re ceptors in the brain have a physiological role in water and electrolyte metabolism.…”

Angiotensin II AT1 receptor antagonists inhibit the angiotensin‐CRF‐AVP axis and are potentially useful for the treatment of stress‐related and mood disorders

“…AVP synthesis in the paraventricular and supraoptic nuclei and its release from the posterior pituitary, to ensure the control of volume homeostasis, retaining water in the kidney and increasing blood pressure during hypovolemia, such as water deprivation and hemorrhage [Fitzsimons, 1998;Reaux et al, 2001;Renaud and Bourque, 1991;Hohle et al, 1995;Meng et al, 1994;Lee et al, 1995;Keil et al, 1983]. Release of AVP is one of the main mechanisms by which brain Ang II increases blood pressure [Phillips, 1997;Severs and Daniels-Severs, 1973;Leng et al, 1992].…”