AJP - Heart Calcium Transients and Cell-Sarcomere
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Am J Physiol Heart Circ Physiol 246: H811-H817, 1984;
0363-6135/84 $5.00
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AJP - Heart and Circulatory Physiology, Vol 246, Issue 6 811-H817, Copyright © 1984 by American Physiological Society


ARTICLES

Delayed reversal of Goldblatt hypertension by angiotensin II infusion in the rat

A. Kumar, R. F. Bing, J. D. Swales and H. Thurston

Reversal of early Goldblatt two-kidney, one-clip hypertension is associated with a fall in plasma renin. To define the role of this in blood pressure normalization we maintained preoperative hypertension for 12 h after unclipping or removal of the ischemic kidney, by angiotensin II or norepinephrine infusions during continuous blood pressure monitoring. High infusion rates of angiotensin II (1 microgram X kg-1 X min-1) were needed to reproduce hypertensive pressures. On stopping angiotensin II there was a rapid initial fall in blood pressure but not to normal (176 +/- 3.1 to 138 +/- 4.3 mmHg at 1 h), and a later slower fall to normal by 24 h (114 +/- 3.9). This response was identical to that of dextrose-infused animals (180 +/- 8.2 to 146 +/- 7.0 at 1 h and 113 +/- 5.6 at 24 h), apart from a transient rise in blood pressure associated with hyperreninemia in unclipped animals 12 h postinfusion. In contrast, after norepinephrine blood pressure fell immediately to normal. Similar responses were seen in normal rats after 12-h pressor infusions of angiotensin II or norepinephrine. These results show that the fast and slow components of the blood pressure fall following reversal of Goldblatt hypertension are delayed but otherwise unaltered specifically by angiotensin II. The need for pharmacologic doses, however, suggests that mechanisms in addition to the direct vasopressor action of angiotensin II are involved.





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