Hypertension, Vol 22, 513-522, Copyright © 1993 by American Heart Association
DJ Campbell, A Kladis and AM Duncan
To determine the contribution of kidney-derived renin and angiotensin
converting enzyme to circulating and tissue levels of angiotensin peptides,
we measured angiotensin (Ang)-(1-7), Ang II, Ang-(1-9), and Ang I in
plasma, kidney, lung, heart, aorta, brown adipose tissue, adrenal,
pituitary, and brain of five groups of male Sprague-Dawley rats: control
rats, rats given the converting enzyme inhibitor ramipril (10 mg/kg), rats
nephrectomized 24 hours, rats nephrectomized 48 hours, and rats
nephrectomized 48 hours and given ramipril. Plasma and tissues, apart from
adrenal, showed a 63% to 98% reduction in Ang II, the ratio of Ang II to
Ang I, or both after ramipril administration, indicating a major role for
converting enzyme in Ang II formation. Nephrectomy caused a more than 95%
decrease in plasma renin levels and a fourfold to eightfold increase in
plasma angiotensinogen levels. Apart from plasma and brain, tissues showed
a 59% to 78% decrease in Ang II levels after nephrectomy, indicating a
major role for kidney- derived renin in Ang II formation. The persistence
of Ang II in plasma and tissues of anephric rats indicates that Ang II may
be formed by a process independent of kidney-derived renin; this process
may be amplified by the increased plasma angiotensinogen levels that
accompany nephrectomy. For lung, adrenal, and aorta, Ang II levels showed a
further decrease when nephrectomized rats were given ramipril. However, for
plasma and the other tissues, ramipril produced little or no decrease in
Ang II levels of anephric rats, suggesting that Ang II may be formed by a
pathway independent of converting enzyme. Such a pathway may involve the
direct formation of Ang II from angiotensinogen by a non-renin-like enzyme.
ARTICLES
Nephrectomy, converting enzyme inhibition, and angiotensin peptides
St Vincent's Institute of Medical Research, Fitzroy, Victoria, Australia.
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