(Hypertension. 2000;35:693.)
© 2000 American Heart Association, Inc.
Editorial |
From Hypertension, Alton Ochsner Medical Foundation, New Orleans, La.
Correspondence to Edward D. Frohlich, MD, Editor-in-Chief, Hypertension, Alton Ochsner Medical Foundation, 1516 Jefferson Hwy, BH 514, New Orleans, LA 70121.
| Introduction |
|---|
Recently, one report appeared in one of the most prestigious weekly
medical journals indicating that angiotensin-converting
enzyme inhibition therapy of patients with chronic renal failure will
reduce "adrenergic hyperactivity."2 The concept
apparently was deemed so novel that an accompanying editorial
commentary was included in that issue of the journal.3 No
references included in either communication referred to the well-known
and well-established phenomenon of angiotensin II
augmentation of adrenergic activity in medullary centers or in
ganglionic function.4 5 Only a few weeks after this
publication, yet another paper was published in a "sister journal"
of the American Heart Association indicating increased sympathetic
nerve activity in patients with renovascular
hypertension.6 Again, no evidence was provided in
This article has been cited by other articles:
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E. D. Frohlich Professor John Douglas Swales Hypertension, May 1, 2001; 37(5): 1198 - 1198. [Full Text] |
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