title: Treatment with irbesartan or atenolol improves endothelial function in essential hypertension.
abstract: OBJECTIVE
  To investigate if antihypertensive treatment could improve endothelium-dependent vasodilatation in hypertensive patients, and whether the angiotensin II subtype-1 (AT1)-receptor antagonist irbesartan and the beta1-receptor antagonist atenolol would differ in this respect.
  
  
  METHODS
  Thirty-four patients (28 men and six women) with mild-to-moderate essential hypertension (diastolic blood pressure 90-120 mmHg) were randomized to once daily 150-300 mg irbesartan or 50-100 mg atenolol in a double-blind fashion, preceded by a placebo run-in period. Forearm blood flow (FBF) was assessed by venous occlusion plethysmography during local intra-arterial infusions of methacholine and sodium nitroprusside, to evaluate endothelium-dependent and endothelium-independent vasodilatation, respectively. Measurements of FBF were undertaken at the end of the run-in placebo period and repeated after 3 months of active antihypertensive treatment.
  
  
  RESULTS
  Irbesartan and atenolol induced a similar decline in blood pressure (from 171/107 to 158/98 mmHg, P < 0.05), and improved endothelium-dependent vasodilatation (e.g. an increase in FBF response to 4 microg/min methacholine from 325 +/- 29% to 411 +/- 41%, P < 0.05), with no difference between the two study drugs. No significant changes in endothelium-independent vasodilatation were induced by irbesartan or by atenolol.
  
  
  CONCLUSIONS
  The present study shows that 3 months of antihypertensive therapy with irbesartan or atenolol improves endothelium-dependent vasodilatation.
authors.affiliation: Department of Internal Medicine, University Hospital, Uppsala, Sweden. bengt.muhlen@medsci.uu.se
authors.forename: B
authors.initials: B
authors.lastname: von zur Mühlen
authors.forename: T
authors.initials: T
authors.lastname: Kahan
authors.forename: A
authors.initials: A
authors.lastname: Hägg
authors.forename: J
authors.initials: J
authors.lastname: Millgård
authors.forename: L
authors.initials: L
authors.lastname: Lind
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use*; D057911:Angiotensin Receptor Antagonists; D000959:Antihypertensive Agents / Q000627:therapeutic use*; D001262:Atenolol / Q000627:therapeutic use*; D001713:Biphenyl Compounds / Q000627:therapeutic use*; D004311:Double-Blind Method; D004730:Endothelium, Vascular / Q000187:drug effects* / Q000503:physiopathology*; D005260:Female; D005542:Forearm / Q000098:blood supply; D006801:Humans; D006973:Hypertension / Q000188:drug therapy* / Q000503:physiopathology*; D000077405:Irbesartan; D008297:Male; D008875:Middle Aged; D044140:Receptor, Angiotensin, Type 1; D012039:Regional Blood Flow / Q000187:drug effects; D013777:Tetrazoles / Q000627:therapeutic use*; D014664:Vasodilation / Q000187:drug effects
chemical_list: D000319:Adrenergic beta-Antagonists; D057911:Angiotensin Receptor Antagonists; D000959:Antihypertensive Agents; D001713:Biphenyl Compounds; D044140:Receptor, Angiotensin, Type 1; D013777:Tetrazoles; D001262:Atenolol; D000077405:Irbesartan