Chest ACCP Member Benefits
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     

Guest Access | Sign In via User Name/Password
This Article
Right arrow Full Text (PDF) Free
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Article Archive
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Mathias, C. J.
Right arrow Articles by Snell, M. E.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Mathias, C. J.
Right arrow Articles by Snell, M. E.
(Chest. 1983;83:357-359.)
© 1983 American College of Chest Physicians

Clonidine Lowers Blood Pressure Independently of Renin Suppression in Patients with Unilateral Renal Artery Stenosis

C. J. Mathias M.D.1; A. Wilkinson M.D.1; P. S. Lewis M.D.1; W. S. Peart M.D.1; P. S. Sever M.D.1; and M. E. Snell M.D.1

1 From the Departments of Medicine, Clinical Pharmacology, and Surgery, St. Mary's Hospital Medical School, University of London, England

The effects of 300 µg of oral clonidine were studied in nine patients with unilateral renal artery stenosis proved by selective renal arteriography. Blood pressure, heart rate, plasma renin activity (PRA) levels, plasma noradrenaline levels, and sedation were measured before and for eight hours after dosage. After clonidine administration, both systolic and diastolic blood pressure fell within the first hour, was maximum in the fourth hour, and remained lower than predosage levels even in the eighth hour. There was a fall in heart rate, maximum in the fourth hour. There were minimal changes in PRA levels after giving the clonidine. Plasma noradrenaline levels fell, with the maximum fall in the sixth hour. Sedation occurred within one hour of dosage and was maximum in the second hour. We conclude that in patients with unilateral renal artery stenosis clonidine causes a substantial and prolonged fall in blood pressure not accompanied by suppression of PRA levels but by a reduction in plasma noradrenaline levels. This suggests a role for central pressor mechanisms, probably linked to angiotensin II and central sympathetic activation, in the maintenance of hypertension in patients with renal artery stenosis.







HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1983 by the American College of Chest Physicians.