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Ultrasound Assessment of Endothelial-Dependent Flow-Mediated Vasodilation of the Brachial Artery in Clinical Research
08:42

Ultrasound Assessment of Endothelial-Dependent Flow-Mediated Vasodilation of the Brachial Artery in Clinical Research

Published on: October 22, 2014

Reversal of glibenclamide-induced coronary vasoconstriction by enhanced perfusion pulsatility: possible role for

P Pagliaro1, N Paolocci, T Isoda

  • 1Department of Medicine, Johns Hopkins Medical Institutions, Baltimore, MD 21287, USA.

Cardiovascular Research
|March 23, 2000
PubMed

Insights

Increased blood flow pulsatility counteracts coronary artery constriction from ATP-sensitive potassium (K+ATP) channel blockade, likely via nitric oxide (NO) release. This mechanism may aid exercise-induced dilation when K+ATP channels are compromised.

Area of Science:

  • Cardiovascular Physiology
  • Vascular Biology
  • Pharmacology

Background:

  • ATP-sensitive potassium (K+ATP) channels influence basal coronary tone.
  • Glibenclamide (GLI) blockade of K+ATP channels does not affect exercise-induced coronary flow reserve.
  • Exercise increases coronary perfusion pulsatility.

Purpose of the Study:

  • To test if increased perfusion pulsatility offsets K+ATP channel-mediated vasoconstriction.
  • To investigate if nitric oxide synthase (NOS) inhibition blunts this compensatory effect.
  • To determine if this pulsatility effect is specific to K+ATP channel blockade.

Main Methods:

  • Anesthetized dogs with computer-controlled coronary artery perfusion.
  • Varied perfusion pulse pressure (PP) from 40 to 100 mm Hg.
  • Administered glibenclamide (GLI), NG-monomethyl-L-arginine (L-NMMA), vasopressin, and quinacrine.

Main Results:

  • GLI-induced vasoconstriction was abolished at high PP (100 mm Hg) but present at low PP (40 mm Hg).
  • NOS inhibition blunted the pulsatility-induced flow augmentation and acetylcholine-induced dilation.
  • Vasopressin and quinacrine caused vasoconstriction that was not offset by increased pulsatility.

Conclusions:

  • Increased coronary flow pulsatility likely enhances nitric oxide (NO) release, offsetting K+ATP channel blockade.
  • This pulsatility-mediated NO release may be a key mechanism supporting exercise hyperemia.
  • The findings suggest a protective role for pulsatility in maintaining coronary flow during compromised K+ATP channel function.
Abstract

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