Regulation of myocyte contraction via neuronal nitric oxide synthase: role of ryanodine receptor S-nitrosylation (pages 2905–2917)
Honglan Wang, Serge Viatchenko-Karpinski, Junhui Sun, Inna Györke, Nancy A. Benkusky, Mark J. Kohr, Héctor H. Valdivia, Elizabeth Murphy, Sandor Györke and Mark T. Ziolo
Article first published online: 3 AUG 2010 | DOI: 10.1113/jphysiol.2010.192617
Nitric oxide (NO) is an important regulator of cardiac contraction. NO produced via the neuronal isoform of NO synthase (NOS1) leads to enhanced contraction. We show that part of the enhanced contraction via NOS1 is through the modulation of the sarcoplasmic reticulum Ca2+ release channel (ryanodine receptor). Specifically, we find that NOS1 leads to S-nitrosylation and increased activity of the ryanodine receptor. We further show that the increased ryanodine receptor activity by NOS1 contributes to the enhanced contraction. These results reveal a mechanism of how NOS1 modulates cardiac contraction and helps us understand how NO influences cardiac function.