Key result
Nitric oxide appears to modulate the function of the cardiac ryanodine receptor Ca(2+) release channel, potentially contributing to altered contractility in heart failure.
Design
Review
Authors
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NO may modulate RyR2 in ECC; leaves open its physiological or therapeutic relevance.
This review highlights the complex modulatory effects of nitric oxide on cardiac ryanodine receptors, suggesting that altered NO signaling may contribute to abnormal calcium handling in heart failure.
Lim et al. (2007) conducted a review in Heart failure. Nitric oxide was evaluated. Nitric oxide appears to modulate the function of the cardiac ryanodine receptor Ca(2+) release channel, potentially contributing to altered contractility in heart failure.
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