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(Hypertension. 2001;38:23.)
© 2001 American Heart Association, Inc.
Scientific Contributions |
From the Department of Medicine, Osaka City General Hospital (M.I.), and the National Cardiovascular Center, Suita (T.T., S.N., M.T.), Osaka, Japan.
Correspondence to Masahito Imanishi, MD, Department of Medicine, Osaka City General Hospital, 2-13-22 Miyakojima-hondori, Miyakojima-ku, Osaka 534-0021, Japan. E-mail masachan{at}msic.med.osaka-cu.ac.jp
Abstract Differences between prostaglandins I2 and E2 in their renal synthesis and pathophysiological roles were investigated in unilateral renovascular hypertension of different severities in 18 patients: 6 with mild stenosis (<75% of the diameter) of the renal artery, 7 with moderate stenosis (75% to 90%), and 5 with severe stenosis (>90%). Before and after aspirin administration (10 mg/kg), renal venous and aortic plasma was assayed for 6-ketoprostaglandin F1
(instead of prostaglandin I2), prostaglandin E2, and renin activity. In mild or moderate stenosis, the mean 6-ketoprostaglandin F1
level in renal venous plasma from the stenotic side was not different from that from the normal side or from aortic plasma. Prostaglandin E2 levels and renin activity in such patients were higher on the stenotic side than on the normal side and higher in venous than in aortic plasma. Aspirin inhibited prostaglandin E2 synthesis and suppressed renin release from stenotic kidneys and lowered blood pressure as the renin activity decreased in patients with mild or moderate stenosis. In severe stenosis, levels of 6-ketoprostaglandin F1
and prostaglandin E2 were higher on the stenotic side than on the normal side and higher in venous than in aortic plasma. Aspirin inhibited the synthesis of both prostaglandins and suppressed renin release from the stenotic kidney. In patients with unilateral renovascular hypertension with mild or moderate stenosis of the renal artery, prostaglandin E2, rather than I2, seems to contribute to further acceleration of renin release. Prostaglandin I2 may increase and participate in further renin release when the stenosis is severe.
Key Words: prostaglandins hypertension, renovascular kidney
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