title: Differences between the effects of metoprolol and prazosin on the forearm vasculature in primary hypertension.
abstract: OBJECTIVE
  To study the forearm vascular resistance in patients at rest and during ischaemia and cardiovascular responses to noradrenaline infusions during treatment with a beta1-adrenoceptor antagonist, metoprolol, and with an alpha1-adrenoceptor antagonist, prazosin.
  
  
  METHODS
  Eighteen previously untreated primary hypertension patients were selected for therapy either with 50-250 mg/day metoprolol (n = 11) or with 3-20 mg/day prazosin (n = 8).
  
  
  METHODS
  The minimal vascular resistance after ischaemic work was calculated from the forearm blood flow determined by venous occlusion plethysmography before treatment and after two and 16 months of treatment Arterial and venous plasma noradrenaline levels were determined and systemic pressor responses and forearm vasoconstriction were studied during intravenous infusion of noradrenaline.
  
  
  RESULTS
  The resting mean arterial pressure was reduced differently by metoprolol and prazosin (by 20% versus by 8%; P < 0.001 for difference). The minimal vascular resistance decreased similarly after 16 months of metoprolol (17% decrease; P < 0.05) and of prazosin (24% decrease; P < 0.05) treatments. Arterial noradrenaline levels increased after 16 months of metoprolol treatment and after 2 and 16 months of prazosin treatment. The forearm noradrenaline spillover was reduced after 16 months on prazosin, but remained unchanged during metoprolol treatment. Pressor responses to intravenous noradrenaline were affected little by either treatment, whereas reflexogenic bradycardia was attenuated by prazosin treatment.
  
  
  CONCLUSIONS
  The findings suggest that metoprolol and prazosin treatments reduce the minimal vascular resistance similarly, despite different reductions in blood pressure. Prazosin treatment might also reduce the forearm sympathetic nerve activity. Reductions in minimal forearm vascular resistance during antihypertensive therapy need not be related only to the lowering of the blood pressure per se.
authors.affiliation: Department of Medicine, St Göran's Hospital, Stockholm, Sweden.
authors.forename: I
authors.initials: I
authors.lastname: Gretzer
authors.forename: P
authors.initials: P
authors.lastname: Hjemdahl
mesh_terms: D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology*; D000319:Adrenergic beta-Antagonists / Q000494:pharmacology*; D000328:Adult; D002395:Catecholamines / Q000097:blood; D005260:Female; D005542:Forearm / Q000098:blood supply*; D006439:Hemodynamics / Q000187:drug effects; D006801:Humans; D006973:Hypertension / Q000503:physiopathology*; D007511:Ischemia / Q000503:physiopathology; D008297:Male; D008790:Metoprolol / Q000494:pharmacology*; D009638:Norepinephrine / Q000494:pharmacology; D011224:Prazosin / Q000494:pharmacology*; D014655:Vascular Resistance / Q000187:drug effects*; D014664:Vasodilation / Q000187:drug effects
chemical_list: D000317:Adrenergic alpha-Antagonists; D000319:Adrenergic beta-Antagonists; D002395:Catecholamines; D008790:Metoprolol; D009638:Norepinephrine; D011224:Prazosin