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Treatment with irbesartan or atenolol improves endothelial function in essential hypertension

B von zur Mühlen1, T Kahan, A Hägg

  • 1Department of Internal Medicine, University Hospital, Uppsala, Sweden. bengt.muhlen@medsci.uu.se

Journal of Hypertension
|October 11, 2001
PubMed

Insights

Antihypertensive treatments with irbesartan or atenolol significantly improved endothelium-dependent vasodilation in hypertensive patients. Both drugs demonstrated comparable efficacy in enhancing blood vessel function.

Area of Science:

  • Cardiovascular Medicine
  • Pharmacology

Background:

  • Essential hypertension is characterized by impaired endothelium-dependent vasodilation.
  • The role of specific antihypertensive agents in improving endothelial function requires further investigation.

Purpose of the Study:

  • To compare the effects of irbesartan (angiotensin II subtype-1 receptor antagonist) and atenolol (beta1-receptor antagonist) on endothelium-dependent vasodilation in hypertensive patients.
  • To determine if antihypertensive treatment can restore normal endothelial function.

Main Methods:

  • A double-blind, randomized study involving 34 patients with mild-to-moderate essential hypertension.
  • Patients received either irbesartan or atenolol for 3 months after a placebo run-in period.
  • Forearm blood flow was measured using venous occlusion plethysmography during methacholine and sodium nitroprusside infusions to assess endothelium-dependent and independent vasodilation, respectively.

Main Results:

  • Both irbesartan and atenolol effectively lowered blood pressure similarly.
  • A significant improvement in endothelium-dependent vasodilation was observed with both drugs, with no significant difference between them.
  • No significant changes in endothelium-independent vasodilation were noted with either treatment.

Conclusions:

  • Three months of antihypertensive therapy with either irbesartan or atenolol improves endothelium-dependent vasodilation in hypertensive patients.
  • These findings suggest that targeting the renin-angiotensin system or beta-adrenergic receptors can positively impact endothelial function.
Abstract

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