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Reprint of: the paradox of α-adrenergic coronary vasoconstriction revisited

Gerd Heusch1

  • 1Institut für Pathophysiologie, Universitätsklinikum Essen, Hufelandstr. 55, 45122 Essen, Germany. gerd.heusch@uk-essen.de

Journal of Molecular and Cellular Cardiology
|March 17, 2012
PubMed

Insights

Activation of coronary vascular alpha-adrenoceptors causes vasoconstriction, hindering blood flow. Blocking these receptors improves coronary blood flow, benefiting patients with coronary artery disease.

Area of Science:

  • Cardiovascular Physiology
  • Pharmacology

Background:

  • Coronary vascular alpha-adrenoceptors mediate vasoconstriction, opposing metabolic vasodilation during sympathetic activation.
  • Alpha(1)-adrenoceptors primarily mediate epicardial vessel constriction, while alpha(2)-adrenoceptors, along with alpha(1), constrict the microcirculation.

Purpose of the Study:

  • To evaluate the role of alpha-adrenergic coronary vasoconstriction in regulating blood flow.
  • To assess the effects of alpha-adrenoceptor blockade on coronary blood flow and myocardial function.

Main Methods:

  • Review of existing literature on alpha-adrenergic receptor function in coronary circulation.
  • Analysis of studies involving alpha-blockade in animal models and human patients.

Main Results:

  • Alpha-adrenergic vasoconstriction does not beneficially affect transmural blood flow distribution.
  • Alpha-blockade improves blood flow to all transmural layers in dogs under various perfusion conditions.
  • Blockade of alpha(1)- and alpha(2)-adrenoceptors enhances coronary blood flow, myocardial function, and metabolism in patients with coronary artery disease.

Conclusions:

  • Alpha-adrenergic coronary vasoconstriction is detrimental to blood flow distribution.
  • Alpha-adrenoceptor blockade represents a potential therapeutic strategy for improving coronary circulation and cardiac function, particularly in coronary artery disease.

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