Circulation, Vol 74, 1203-1207, Copyright © 1986 by American Heart Association
MT Olivari, TB Levine and JN Cohn
The reduced responsiveness of the renin-angiotensin system to hemodynamic
changes in patients with congestive heart failure (CHF) could be due to a
defect of the juxtaglomerular apparatus. To test this hypothesis, the
responses to viprostol, an analog of prostaglandin E2 (PGE2) that is known
to stimulate both the macula densa and the juxtaglomerular cells, and to
nitroprusside were compared in patients with CHF. An average fall in mean
arterial pressure (MAP) of 6 mm Hg with viprostol was associated with a
fivefold increase in plasma renin activity (PRA) from 11.4 +/- 6.4 to 47.9
+/- 31.0 ng/ml/hr; in contrast PRA did not change with nitroprusside,
despite a significant decrease in preload and an average decrease in MAP of
16 mm Hg. These data demonstrate that the renin-angiotensin system could be
activated by PGE2 in patients with CHF, this activation is not related to
the global hemodynamic changes induced by PGE2, and the previously reported
unresponsiveness of the renin-angiotensin system in patients with CHF
cannot be attributed to a defective response of the juxtaglomerular
apparatus.
ARTICLES
Evidence for a direct renal stimulating effect of prostaglandin E2 on renin release in patients with congestive heart failure
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