THERAPEUTIC CLASS

Nitric oxide and cardiac function

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Nitric oxide (NO) participates in the control of contractility and heart rate, limits cardiac remodeling after an infarction and contributes to the protective effect of ischemic pre- and postconditioning. Low concentrations of NO, with production of small amounts of cGMP, inhibit phosphodiesterase III, thus preventing the hydrolysis of cAMP. The subsequent activation of a protein-kinase A causes the opening of sarcolemmal voltage-operated and sarcoplasmic ryanodin receptor Ca2+ channels, thus increasing myocardial contractility

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: .,

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Language

English

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Classification

NONE

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Subject(s)

Cardiovascular & Hematopoietic System
NTG

Specific Detail Info

Life Sciences 81 (2007) 779–793

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