title: Increased cardiac sympathetic drive in renovascular hypertension.
abstract: BACKGROUND
  Patients with renovascular hypertension (RVH) have high cardiovascular mortality and morbidity. In these patients, overall sympathetic nerve activity is increased. It is unknown, however, whether this increase also involves the heart.
  
  
  OBJECTIVE
  We tested the hypothesis that cardiac sympathetic activity is increased in patients with hypertension and renal artery stenosis.
  
  
  RESULTS
  A total of 14 patients with hypertension were studied before angioplasty of angiographically identified renal artery stenosis. Nine out of 14 patients had renovascular hypertension proven at the 1-year follow-up visit. A total of 19 healthy subjects served as a control group. A right heart catheterization, including the positioning of a coronary sinus thermodilution catheter was performed for hemodynamic recordings and blood sampling. Using a radiotracer dilution technique with infusion of tritiated noradrenaline ([3H]NA) and adrenaline ([3H]A), fractional extraction and clearance were calculated. Total body and cardiac NA spillovers were used as indices of systemic and cardiac sympathetic nervous activity. The study group had normal left ventricular ejection fraction and cardiac pressures. Cardiac NA spillover was increased by 127% in the hypertensive patients compared with healthy subjects (200 +/- 53 versus 88 +/- 10 pmol/min in controls, P < 0.05). Total body NA spillover was similar in both groups. Cardiac fractional extraction of [3H]NA and [3H]A was decreased by 26 and 47%, respectively, compared with normotensive subjects (P < 0.01 for both).
  
  
  CONCLUSIONS
  Patients with renovascular hypertension have altered cardiac sympathetic function with increased sympathetic drive and impaired catecholamine extraction. The increased cardiac sympathetic drive may have adverse long-term effects on prognosis in this patient group with high cardiovascular mortality.
authors.affiliation: Department of Cardiology, Sahlgrenska University Hospital, Göteborg, Sweden. magnus.petersson@hjl.gu.se
authors.forename: Magnus J
authors.initials: MJ
authors.lastname: Petersson
authors.forename: Bengt
authors.initials: B
authors.lastname: Rundqvist
authors.forename: Mats
authors.initials: M
authors.lastname: Johansson
authors.forename: Graeme
authors.initials: G
authors.lastname: Eisenhofer
authors.forename: Gavin
authors.initials: G
authors.lastname: Lambert
authors.forename: Hans
authors.initials: H
authors.lastname: Herlitz
authors.forename: Gert
authors.initials: G
authors.lastname: Jensen
authors.forename: Peter
authors.initials: P
authors.lastname: Friberg
mesh_terms: D003326:Coronary Circulation; D004837:Epinephrine / Q000097:blood / Q000493:pharmacokinetics; D005260:Female; D006329:Heart Conduction System / Q000503:physiopathology*; D006801:Humans; D006978:Hypertension, Renovascular / Q000378:metabolism / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D009638:Norepinephrine / Q000097:blood / Q000493:pharmacokinetics; D017534:Radial Artery; D012016:Reference Values; D013564:Sympathetic Nervous System / Q000503:physiopathology*
chemical_list: D009638:Norepinephrine; D004837:Epinephrine