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Inhibiting angiotensin type 1 receptors as a target for diabetes

Ulrich Kintscher1, Anna Foryst-Ludwig, Thomas Unger

  • 1Charité-Universitätsmedizin Berlin, Institute of Pharmacology, Center for Cardiovascular Research, Hessische Street, 3-4, 10115 Berlin, Germany. ulrich.kintscher@charite.de

Expert Opinion on Therapeutic Targets
|September 11, 2008
PubMed

Insights

Angiotensin type 1 receptor blockers (ARBs) may prevent type 2 diabetes and reduce cardiovascular risks in diabetic patients. The study compares ARBs with ACE inhibitors and explores ARBs with PPARgamma activation for improved outcomes.

Area of Science:

  • Cardiovascular Medicine
  • Endocrinology
  • Pharmacology

Background:

  • Angiotensin type 1 (AT1) receptor blockers (ARBs) treat hypertension and associated end-organ damage.
  • ARBs influence glucose and lipid metabolism, with trials showing reduced type 2 diabetes risk compared to other antihypertensives.
  • AT1 receptor blockade lowers cardiovascular morbidity and mortality in diabetic populations, though mechanisms remain unclear.

Purpose of the Study:

  • To determine if selective AT1 receptor blockade is superior to ACE inhibition in preventing diabetes and reducing cardiovascular endpoints in diabetic patients.
  • To assess if an ARB with PPARgamma-activating properties offers advantages over one without this action.

Main Methods:

  • The study discusses findings from the Ongoing Telmisartan Alone and in Combination with Ramipril Global End point Trial (ONTARGET).

Main Results:

  • ONTARGET provides data to address the clinical questions regarding AT1 receptor blockade in diabetes management.
  • The trial's results are crucial for understanding the comparative efficacy of different antihypertensive strategies in diabetic patients.

Conclusions:

  • The ONTARGET trial offers critical insights into the role of AT1 receptor blockers in managing diabetes and cardiovascular risk.
  • Findings inform clinical practice regarding the choice between selective AT1 receptor blockade and ACE inhibition, and the significance of PPARgamma activation.
Abstract

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