title: The sympathetic nervous system in hypertension due to unilateral renal artery stenosis in man.
abstract: 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)
authors.affiliation: Department of Medicine, St Mary's Hospital Medical School/Imperial College, London, UK.
authors.forename: J S
authors.initials: JS
authors.lastname: Kooner
authors.forename: W S
authors.initials: WS
authors.lastname: Peart
authors.forename: C J
authors.initials: CJ
authors.lastname: Mathias
mesh_terms: D000328:Adult; D000368:Aged; D000450:Aldosterone / Q000097:blood; D001794:Blood Pressure / Q000502:physiology; D002216:Captopril / Q000494:pharmacology; D003000:Clonidine / Q000494:pharmacology; D005260:Female; D005542:Forearm / Q000098:blood supply; D006339:Heart Rate / Q000502:physiology; D006439:Hemodynamics / Q000502:physiology; D006801:Humans; D006978:Hypertension, Renovascular / Q000209:etiology / Q000503:physiopathology* / Q000601:surgery; D008297:Male; D008875:Middle Aged; D012039:Regional Blood Flow / Q000502:physiology; D012078:Renal Artery Obstruction / Q000150:complications / Q000503:physiopathology*; D012083:Renin / Q000097:blood; D012867:Skin / Q000098:blood supply; D012881:Skin Temperature / Q000502:physiology; D013564:Sympathetic Nervous System / Q000503:physiopathology*; D014655:Vascular Resistance / Q000502:physiology
chemical_list: D000450:Aldosterone; D002216:Captopril; D012083:Renin; D003000:Clonidine