Key result
Venous plasma levels of UTP were increased by 57% in patients with myocardial infarction, and pyrimidines demonstrated positive inotropic effects on cardiomyocytes via P2Y2 and P2Y6 receptors.
Extracellular pyrimidines (UTP and UDP) act as cardiac inotropic factors via P2Y2 and P2Y6 receptors and are released during myocardial infarction in humans.
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May identify novel inotropic pathway in MI; animal data leave therapeutic targeting open for human study.
Wihlborg et al. (2006) studied Myocardial infarction. Extracellular pyrimidines (UTP and UDP) was evaluated on Venous plasma levels of UTP and cardiomyocyte contraction. Venous plasma levels of UTP were increased by 57% in patients with myocardial infarction, and pyrimidines demonstrated positive inotropic effects on cardiomyocytes via P2Y2 and P2Y6 receptors.
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