TY - JOUR
T1 - Role of angiotensin in thirst
AU - Rolls, Barbara J.
AU - Wood, R. J.
N1 - Funding Information:
ACKNOWLEDGEMENTS This work was supported by tile Medical Research Council. We wish to thank Dr. A.W. Castellion of Norwich Pbarmacal for supplying the saralasin acetate.
Copyright:
Copyright 2014 Elsevier B.V., All rights reserved.
PY - 1977/3
Y1 - 1977/3
N2 - Angiotensin is a potent dipsogenic substance and causes elevated water intake in some pathological conditions but as yet no physiological role for angiotensin in normal thirst has been proven. If angiotensin is important in normal drinking, then it should contribute to the drinking which follows water deprivation. The rehydration of bilaterally nephrectomized rats, rats with bilateral ureteric ligation and control rats was compared after 21 hours of water deprivation. The total intake during the 6 hour rehydration was the same in the 3 groups despite the differences in the level of circulating angiotensin. Thus the renal renin-angiotensin system is not essential for deprivation-induced drinking. Another way to test any contribution to drinking by angiotensin is the administration of the competitive angiotensin inhibitor, saralasin acetate. In a control experiment saralasin acetate was found to block the dipsogenic effect of intravenous angiotensin. The infusion of saralasin acetate in a wide range of doses did not, however, affect the drinking following ligation of the inferior vena cava. Thus angiotensin is not essential for drinking following caval ligation. Two possible explanations for these results are that angiotensin is not normally involved in these types of thirst or that there is redundancy in the control of drinking with compensation for blocked mechanisms.
AB - Angiotensin is a potent dipsogenic substance and causes elevated water intake in some pathological conditions but as yet no physiological role for angiotensin in normal thirst has been proven. If angiotensin is important in normal drinking, then it should contribute to the drinking which follows water deprivation. The rehydration of bilaterally nephrectomized rats, rats with bilateral ureteric ligation and control rats was compared after 21 hours of water deprivation. The total intake during the 6 hour rehydration was the same in the 3 groups despite the differences in the level of circulating angiotensin. Thus the renal renin-angiotensin system is not essential for deprivation-induced drinking. Another way to test any contribution to drinking by angiotensin is the administration of the competitive angiotensin inhibitor, saralasin acetate. In a control experiment saralasin acetate was found to block the dipsogenic effect of intravenous angiotensin. The infusion of saralasin acetate in a wide range of doses did not, however, affect the drinking following ligation of the inferior vena cava. Thus angiotensin is not essential for drinking following caval ligation. Two possible explanations for these results are that angiotensin is not normally involved in these types of thirst or that there is redundancy in the control of drinking with compensation for blocked mechanisms.
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U2 - 10.1016/0091-3057(77)90020-X
DO - 10.1016/0091-3057(77)90020-X
M3 - Article
C2 - 857251
AN - SCOPUS:0017363664
SN - 0091-3057
VL - 6
SP - 245
EP - 250
JO - Pharmacology, Biochemistry and Behavior
JF - Pharmacology, Biochemistry and Behavior
IS - 3
ER -