Pharmacology

Original Paper

Centrally Mediated Hydration Effects of Angiotensin in Various States of Sodium Balance

Kapsha J.M. · Keil L.C. · Klase P.A. · Severs W.B.

Author affiliations

Department of Pharmacology, The Milton S. Hershey Medical Center, Pennsylvania State University, College of Medicine, Hershey, Pa., and Biomedical Research Division, NASA, Ames Research Center, Moffett Field, Calif.

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Pharmacology 1979;18:25–33

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Article / Publication Details

First-Page Preview
Abstract of Original Paper

Received: March 06, 1978
Accepted: March 27, 1978
Published online: May 29, 2008
Issue release date: 1979

Number of Print Pages: 9
Number of Figures: 0
Number of Tables: 0

ISSN: 0031-7012 (Print)
eISSN: 1423-0313 (Online)

For additional information: https://www.karger.com/PHA

Abstract

Angiotensin, present in the central nervous system and kidneys, affects salt/water balance when administered to either site but the relationship between central and peripheral actions is unclear. One reported difference between central and peripheral administration of the peptide is that the former causes natriuresis whereas the latter conserves sodium. We injected angiotensin II into the lateral cerebroventricles of conscious rats maintained on low, normal and high sodium intakes. Prior to injection, plasma [Na+] and hematocrits were similar in the 3 groups. Angiotensin increased plasma vasopressin content in all groups at 1 and 5 min; the 1-min peak was greater in the high Na+ rats. In control and low Na+ rats plasma renin activity (PRA) was suppressed 5 and 20 min after angiotensin. Basal PRA of high Na+ rats was low and tended to be further suppressed by angiotensin. Angiotensin-induced water intake was similar in all groups. Thus, the response pattern to intraventricular angiotensin (vasopressin release, PRA suppression and drinking behavior) occurred over a range of sodium intakes sufficient to suppress or elevate basal PRA. These responses, and the natriuretic effect of intraventricular angiotensin, would be beneficial under conditions of Na+ excess. Conversely, these effects would be detrimental in Na+-defícient conditions since they reduce the ability to maintain extracellular [Na+]. Angiotensin effects in brain may be increased by sodium excess whereas the renal angiotensin system is utilized in response to Na+ deficiency.

© 1979 S. Karger AG, Basel




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Article / Publication Details

First-Page Preview
Abstract of Original Paper

Received: March 06, 1978
Accepted: March 27, 1978
Published online: May 29, 2008
Issue release date: 1979

Number of Print Pages: 9
Number of Figures: 0
Number of Tables: 0

ISSN: 0031-7012 (Print)
eISSN: 1423-0313 (Online)

For additional information: https://www.karger.com/PHA


Copyright / Drug Dosage / Disclaimer

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Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug.
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