Document Detail

The sympathetic nervous system in hypertension due to unilateral renal artery stenosis in man.
MedLine Citation:
PMID:  1822252     Owner:  NLM     Status:  MEDLINE    
The contribution of neurogenic mechanisms in maintaining hypertension was investigated in 13 patients with unilateral renal artery stenosis (twelve with normal, one with grossly elevated plasma renin levels) by determining the haemodynamic and hormonal responses to the centrally acting sympatholytic agent, clonidine. The same patients were studied after captopril to determine the dependency of their blood pressure on the direct peripheral effects of angiotensin-II. Sixteen patients with essential hypertension (normal plasma renin) were additionally studied after clonidine. After clonidine, blood pressure fell markedly in patients with renal artery stenosis (17 +/- 3%) and essential hypertension (18 +/- 2%). In both groups, clonidine lowered cardiac output by a reduction in stroke volume and heart rate; forearm vascular resistance was unchanged but digital skin vascular resistance fell. Plasma noradrenaline levels were normal in both groups and fell after clonidine; plasma renin activity and aldosterone levels were unchanged. After captopril, blood pressure fell minimally (5 +/- 3%) in renal artery stenosis patients; cardiac output fell and forearm and digital skin vascular resistance were unchanged. Plasma renin activity rose, plasma aldosterone fell and plasma noradrenaline was unchanged after captopril. In the patient with grossly elevated renin levels, blood pressure fell minimally (6%) after clonidine, but unlike others fell profoundly (37%) after captopril. We conclude that, in the majority of our renal artery stenosis patients, despite the elevated blood pressure, sympathetic nervous activity was not reduced. Central neurogenic mechanisms appear to play an important role in maintaining raised blood pressure. In the same patients the peripheral effects of angiotensin-II did not maintain vascular tone or hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)
J S Kooner; W S Peart; C J Mathias
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Clinical autonomic research : official journal of the Clinical Autonomic Research Society     Volume:  1     ISSN:  0959-9851     ISO Abbreviation:  Clin. Auton. Res.     Publication Date:  1991 Sep 
Date Detail:
Created Date:  1992-08-31     Completed Date:  1992-08-31     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  9106549     Medline TA:  Clin Auton Res     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  195-204     Citation Subset:  IM    
Department of Medicine, St Mary's Hospital Medical School/Imperial College, London, UK.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Aldosterone / blood
Blood Pressure / physiology
Captopril / pharmacology
Clonidine / pharmacology
Forearm / blood supply
Heart Rate / physiology
Hemodynamics / physiology
Hypertension, Renovascular / etiology,  physiopathology*,  surgery
Middle Aged
Regional Blood Flow / physiology
Renal Artery Obstruction / complications,  physiopathology*
Renin / blood
Skin / blood supply
Skin Temperature / physiology
Sympathetic Nervous System / physiopathology*
Vascular Resistance / physiology
Reg. No./Substance:
4205-90-7/Clonidine; 52-39-1/Aldosterone; 62571-86-2/Captopril; EC

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

Previous Document:  Biochemical evidence of sympathetic denervation of the heart in pure autonomic failure.
Next Document:  Circulatory autonomic failure 50 years after acute poliomyelitis.