Intracerebroventricular captopril does not inhibit osmotically stimulated vasopressin release.

Experiments were carried out to determine the effect of intracerebroventricular (icv) administration of the angiotensin-converting enzyme inhibitor, captopril, on osmotically stimulated vasopressin secretion. During icv infusion of captopril (3.1 micrograms/kg . min), dogs were infused intravenously (iv) with either 2.5 or 0.15 M NaCl. Control groups received an osmotically equivalent mannitol solution icv with the 2.5 or 0.15 M NaCl iv infusion. As a result of the iv hypertonic saline infusion, plasma vasopressin concentrations increased progressively and in concert with the plasma osmolality; this response was not altered by icv captopril. Plasma vasopressin levels were unchanged during iv isotonic saline infusion, and, again, icv captopril was without effect. At the completion of the icv infusions, injection of angiotensin I icv (310 ng/kg) produced a markedly greater increase in plasma vasopressin levels in animals which had received mannitol icv, compared to those which had received captopril icv. On the basis of these findings, a role for an intrinsic brain renin-angiotensin system, if such a system exists, in the osmotic control of vasopressin secretion is seriously questioned, but not ruled out.