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Accelerated Induction of Two-Kidney Hypertension in Rats and Renin-Angiotensin Sensitivity

Studies were performed to substantiate the hypothesis that a physiological change, apart from the rise in blood pressure, occurs in two-kidney hypertensive rats. Both the slow development of hypertension following renal arterial constriction versus its rapid reversal following removal of the constri...

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Bibliographic Details
Published in:Circulation research 1974-11, Vol.35 (5), p.734-741
Main Authors: SKULAN, THOMAS W, Brousseau, Armand C, Leonard, Kathleen A
Format: Article
Language:English
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Summary:Studies were performed to substantiate the hypothesis that a physiological change, apart from the rise in blood pressure, occurs in two-kidney hypertensive rats. Both the slow development of hypertension following renal arterial constriction versus its rapid reversal following removal of the constriction and the early increase in plasma renin activity which subsides in the chronic hypertensive phase suggest such a progressive change. We studied the development of hypertension following initial renal arterial constriction (clipping) and after reclipping in rats that had been relieved of two-kidney hypertension by unclipping for 2 or 21 days. Full hypertensive blood pressure levels were established within 1–2 hours after reclipping in 2-day unclipped rats, but similar levels were not reached in either of the other two groups for at least 1 week. These changes in response to renal arterial constriction were paralleled by differences in responsiveness to hog renin and angiotensin infusions. Plasma renin activity 1 hour after clipping or reclipping was adequate to account for the observed blood pressure increases in all groups. These data suggest that (1) a physiological change resulting in increased vasoresponsiveness to renin and angiotensin occurs concomitantly with the development of two-kidney hypertension and (2) this type of hypertension is dependent on both renin and increased sensitivity to angiotensin. Moreover, we suggest that study of recently unelipped, normotensive rats may help to uncover the causes for the angiotensin sensitivity change.
ISSN:0009-7330
1524-4571
DOI:10.1161/01.RES.35.5.734