Hypertension, Vol 21, 173-184, Copyright © 1993 by American Heart Association
PJ Admiraal, AH Danser, MS Jong, H Pieterman, FH Derkx and MA Schalekamp
To study regional metabolism and production of angiotensin II, we measured
steady-state plasma levels of 125I-angiotensin I and II and endogenous
angiotensin I and II in the aorta and the antecubital, femoral, renal, and
hepatic veins during systemic infusion of 125I- angiotensin I or II.
Extraction of arterially delivered angiotensin II ranged from 30-50% in the
limbs to 80-100% in the renal and hepatomesenteric vascular beds both in
essential hypertension (n = 13) and in unilateral renal artery stenosis (n
= 7). Across the limbs, 20- 30% of arterially delivered angiotensin I was
converted to angiotensin II in both groups, and there was no arteriovenous
gradient in endogenous angiotensin II. No conversion of arterially
delivered angiotensin I was detected across the renal and hepatomesenteric
beds, and there was net extraction of angiotensin II from the systemic
circulation by these beds. Although regional production of angiotensin I at
tissue sites made a significant contribution to its level in the veins,
little of this locally produced angiotensin I reached the regional veins in
the form of angiotensin II, even in the kidney with artery stenosis, where
the venous levels of locally produced angiotensin I were particularly high.
These results provide no evidence for a source of circulating angiotensin
II other than blood-borne angiotensin I and illustrate the high degree of
compartmentalization of angiotensin I and II production.
ARTICLES
Regional angiotensin II production in essential hypertension and renal artery stenosis
Department of Internal Medicine I, University Hospital Dijkzigt, Erasmus University, Rotterdam, The Netherlands.
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