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Platelet nitric oxide signaling system in patients with coronary artery disease

Mahdi Garelnabi1, Vinod Gupta, Venkatesan Mallika

  • 1Department of Clinical Laboratory and Nutritional Sciences, University of Massachusetts Lowell, Massachusetts, USA.

Annals of Vascular Diseases
|April 5, 2013
PubMed

Insights

Platelet nitric oxide (NO) and cyclic guanosine monophosphate (cGMP) levels significantly increase in coronary artery disease (CAD) patients. These elevations may be a compensatory mechanism to reduce platelet activity and calcium levels in CAD.

Area of Science:

  • Cardiovascular Research
  • Biochemistry
  • Platelet Physiology

Background:

  • Coronary artery disease (CAD) is a leading global cause of mortality and hospitalization.
  • The pathogenesis of CAD is closely linked to nitric oxide (NO) production and release.
  • Understanding platelet NO status in CAD is crucial for disease management.

Purpose of the Study:

  • To investigate the status of platelet nitric oxide (NO) in patients with coronary artery disease (CAD).
  • To explore the relationship between NO, cyclic guanosine monophosphate (cGMP), and platelet activity in CAD.

Main Methods:

  • Measured platelet aggregation, cGMP, NO (nitrite/nitrate), NO synthase activity, plasma NO, and ionized calcium (Ca2+).
  • Included 120 CAD patients (myocardial infarction, unstable angina, stable angina) and 40 healthy controls.
  • Subjects' age ranged from 40-51 years.

Main Results:

  • Platelet aggregation, NO, cGMP, NO synthase activity, plasma NO, and ionized Ca2+ were significantly elevated in CAD patients compared to controls (P <0.001).
  • Platelet NO synthase activity and cGMP levels showed marked increases across different CAD patient groups.
  • Specific mean values for NO synthase activity and cGMP levels were reported for each group.

Conclusions:

  • Platelet aggregation, NO, cGMP, NO synthase activity, plasma NO, and ionized Ca2+ are profoundly increased in CAD.
  • Elevated NO-cGMP pathways may represent a compensatory response to mitigate increased platelet activity and calcium levels in CAD.
  • This suggests a complex role for the NO-cGMP system in the pathophysiology of coronary artery disease.
Abstract

Keywords:
cardiovascular diseaseheart diseaseischemic heart diseasenitric oxideplatelets

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