Title

Changes in blood pressure and dipsogenic responsiveness to angiotensin II during chronic exposure of rats to cold

Document Type

Article

Language

eng

Publication Date

4-1991

Publisher

Elsevier

Source Publication

Pharmacology Biochemistry and Behavior

Source ISSN

0091-3057

Abstract

Hypertension accompanies chronic exposure of rats to cold (5–6°C). Systolic, diastolic, and mean blood pressures become elevated, and hypertrophy of the heart occurs. A previous study from this laboratory suggested that the renin-angiotensin system may play a role. The present study was carried out to assess this further. Thus, in addition to measurement of systolic blood pressure at intervals during exposure to cold, plasma renin activity and the dipsogenic responsiveness to acute administration of angiotensin II were also measured to assess the functional status of the renin-angiotensin system. The results showed a significant (p<0.05) increase in systolic blood pressure during the third week of exposure to cold. In contrast, plasma renin activity (PRA) increased within the first week of exposure to cold, and declined thereafter to reach the level of the control by the third week of exposure to cold. By the fourth week, PRA decreased to a level significantly (p<0.05) below that of the control group. The responsiveness to acute administration of angiotensin II (AII), as assessed by the drinking response, increased significantly (p<0.05) by the third week of exposure to cold and remained significantly elevated during the fourth week. There was a significant (p<0.01) direct relationship between dipsogenic responsiveness to AII and blood pressure in the cold-treated (r=.57), but not the control group (r=.12). There was also a significant (r=−.91) indirect linear relationship between PRA and dipsogenic responsiveness to AII. Cold-treated rats had significant increases in urinary norepinephrine output and weights of heart, kidneys, adrenals, and brown adipose tissue characteristic of rats acclimated to cold. Thus, the results suggest, but do not prove, either that the elevation of blood pressure under these conditions may be induced by changes in the renin-angiotensin system or that the same mechanism(s) affects both functions. The results suggest further that the reduction in the drinking response to AII accompanying increases in plasma renin activity may be related to changes in the regulation of central receptors for AII.

Comments

Pharmacology Biochemistry and Behavior, Vol 38, No. 4 (April 1991): 837-842. DOI.

Paula Papanek was affiliated with the University of Florida - Gainesville at the time of publication.

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