Cardiac nitric oxide synthase 1 regulates basal and β-adrenergic contractility in murine ventricular myocytes
Cardiac nitric oxide synthase 1 regulates basal and β-adrenergic contractility in murine ventricular myocytes
复制标题
DOI：
10.1161/01.cir.0000019516.31040.2d
复制
发表时间：
2002-06-25
期刊：
影响因子：
37.8
通讯作者：
Casadei, B
中科院分区：
文献类型：
--
作者：
Ashley, EA;Sears, CE;Casadei, B
Background-Evidence indicates that myocardial NO production can modulate contractility, but the source of NO remains uncertain. Here, we investigated the role of a type 1 NO synthase isoform (NOS1), which has been recently localized to the cardiac sarcoplasmic reticulum, in the regulation of basal and beta-adrenergic myocardial contraction.Methods and Results-Contraction was assessed in left ventricular myocytes isolated from mice with NOS1 gene disruption (NOS1(-/-) mice) and their littermate controls (NOS1(+/+) mice) at 3 stimulation frequencies (1, 3, and 6 Hz) in basal conditions and during beta-adrenergic stimulation with isoproterenol (2 nmol/L). In addition, we examined the effects of acute specific inhibition of NOS1 with vinyl-L-N-5-(1-imino-3-butenyl)-L-ornithine (L-VNIO, 500 mumol/L). NOS I myocytes exhibited greater contraction at all frequencies (percent cell shortening at 6 Hz, 10.7 +/- 0.92% in NOS1(-/-) myocytes versus 7.21+/-1-0.8% in NOS1(+/+) myocytes; P
