Central role of angiotensin in the hyperosmolality- and hypovolaemia-induced vasopressin release in conscious rats

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Abstract
To evaluate a central role of angiotensin in vasopressin (ADH) release in response to hyperosmolality or hypovolemia, in conscious rats the effects of i.p. injections of 2 ml/100 g body wt of hypertonic saline or polyethylene glycol (PEG; 250 mg/ml of 145 mM NaCl) on plasma ADH and angiotensin II (AII) levels and of intracerebroventricular (icv) administrations of Sar1-Ala8-AII (a competitive receptor blocker for AII) on the plasma ADH responses to the i.p. injections were examined. Thirty min after i.p. injections of 900 mM NaCl, plasma ADH, osmolality and Na increased with unchanged plasma AII and with reduced hematocrit. Two h after i.p. administrations of PEG, plasma ADH, AII and hematocrit were augmented with unaltered plasma osmolality and Na. The responses of plasma ADH to i.p. injections of 900 mM NaCl and PEG were significantly inhibited (P < 0.05) by 1 .mu.g of Sar1-Ala8-AII injected icv 5 min before blood samplings which had no appreciable effect on plasma osmolality, electrolytes and hematocrit. Based on these results, angiotensin may participate in both the hyperosmolality- and hypovolemia-induced ADH secretion by acting on the CNS.