AJP - Regulatory, Integrative and Comparative Physiology, Vol 243, Issue 5 558-R562, Copyright © 1982 by American Physiological Society
Angiotensin does contribute to drinking induced by caval ligation in rat
J. T. Fitzsimons and R. M. Elfont
In small (0.5 mg/kg) subcutaneous doses, the angiotensin-converting enzyme
inhibitor, captopril, greatly enhanced drinking in response to caval
ligation in the rat. Drinking was not secondary to urinary water loss since
the rats developed a substantial positive fluid balance. High (50 mg/kg)
subcutaneous doses of captopril reduced drinking to a level below that
following caval ligation alone. This effect could be mimicked by giving
repeated intracerebroventricular injections of captopril (total amount 110
micrograms) to rats treated with the lower subcutaneous dose of captopril.
With this combination, therefore, not only did the lower dose enhancement
disappear, the basal caval ligation drinking response was also reduced with
a total dose of captopril of less than 2% of the higher subcutaneous dose
alone. These results show that, when conversion of angiotensin I to
angiotensin II is prevented in the brain as well as systemically, drinking
in response to caval ligation is reduced although not entirely prevented.
The original report that such drinking is multifactorial, depending on
angiotensin as well as nonangiotensin mechanisms, is confirmed.
