Journal
JAPANESE JOURNAL OF PHYSIOLOGY
Volume 51, Issue 4, Pages 455-461Publisher
CENTER ACADEMIC PUBL JAPAN
DOI: 10.2170/jjphysiol.51.455
Keywords
nitric oxide; contractility; calcium
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We used authentic NO or NO from NO donors to show that the physiological levels of NO (<1 muM) induce a positive inotropic effect and demonstrated that the effect is evoked through a cGMP-dependent pathway. In isolated rat ventricular myocytes, authentic NO at 588 nm increased both cell shortening and the intracellular Ca2+ ([Ca2+](i)) transient (133 and 117%, respectively; p <0.05 vs. baseline), and 0.16-1.7 LM NO elicited reproducible dose-dependent increases in cell shortening. NOC18 (0.1 mm: actual NO concentration 673 nm) or SNAP (0.1 mm: actual NO concentration 285 nM) showed similar effects (shortening 215% and [Ca2+](i) transient 160% increases, and shortening 148% and [Ca2+](i) transient 117% increases, respectively). The NO-induced increases in cell shortening and the [Ca2+](i) transient were inhibited by an inhibitor of soluble guanylate cyclase (ODQ, 30 muM) or by an inhibitor of cAMP-dependent protein kinase (KT5720, 0.1 muM). In the presence of an inhibitor of cGMP-inhibited cAMP-phosphodiesterase (milrinone, 10 muM), NO failed to increase both cell shortening and the [Ca2+](i) transient. These results suggest that physiological levels of NO induce positive inotropy through a cGMP-dependent pathway.
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