Effects of Nitric Oxide Synthase Inhibition on Basal Function and the Force-Frequency Relationship in the Normal and Failing Human Heart In Vivo
Author(s) -
James Cotton,
Mark T. Kearney,
Philip MacCarthy,
Richard M. Grocott-mason,
Dougal R. McClean,
Christophe Heymes,
Peter J. Richardson,
Ajay M. Shah
Publication year - 2001
Publication title -
circulation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.795
H-Index - 607
eISSN - 1524-4539
pISSN - 0009-7322
DOI - 10.1161/hc4401.098515
Subject(s) - medicine , inotrope , contractility , heart failure , cardiology , nitric oxide synthase , dilated cardiomyopathy , nitric oxide , basal (medicine) , omega n methylarginine , cardiomyopathy , heart rate , cardiac function curve , endocrinology , blood pressure , insulin
Nitric oxide (NO) exerts autocrine/paracrine effects on cardiac function, including alterations of the inotropic state. In vitro studies suggest that NO modulates the myocardial force-frequency relationship. Basal left ventricular (LV) contractility is depressed and the force-frequency relationship is blunted in human heart failure, and it is speculated that an increase in NO production is involved.
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