期刊
COMPARATIVE BIOCHEMISTRY AND PHYSIOLOGY A-MOLECULAR & INTEGRATIVE PHYSIOLOGY
卷 142, 期 2, 页码 136-143出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.cbpb.2005.04.012
关键词
cGMP; nitric oxide; cardiac tissue; ion channels; cAMP; cyclic nucleotide phosphodiesterases; cGMP-dependent protein kinase; L-type calcium current
Biochemical studies have established the presence of a NO pathway in the heart, including sources of NO and various effectors. Several cardiac ion channels have been shown to be modified by NO, such as L-type Ca2+, ATP-sensitive K+, and pacemaker f-channels. Some of these effects are mediated by cGMP, through the activity of three main proteins: the cGMP-dependent protein kinase (PKG), the cGMP-stimulated phosphodiesterase (PDE2) and the cGMP-inhibited PDE (PDE3). Other effects appear independent of cGMP, as for instance the NO modulation of the ryanodine receptor-Ca2+ channel. In the case of the cardiac L-type Ca2+ channel current VC,A, both cGMP-dependent and cGMP-independent effects have been reported, with important tissue and species specificity. For instance, in rabbit sinotrial myocytes, NO inhibits the beta-adrenergic stimulation of I-Ca,I-L through activation of PDE2. In cat and human atrial myocytes, NO potentiates the cAMP-dependent stimulation of I-Ca,I-L through inhibition of PDE3. In rabbit atrial myocytes, NO enhances I-Ca,I-L in a cAMP-independent manner through the activation of PKG. In ventricular myocytes, NO exerts opposite effects on I-Ca,I-L: an inhibition mediated by PKG in mammalian myocytes but by PDE2 in frog myocytes; a stimulation attributed to PDE3 inhibition in frog ventricular myocytes but to a direct effect of NO in ferret ventricular myocytes. Finally, NO can also regulate cardiac ion channels by a direct action on G-proteins and adenylyl cyclase. (C) 2005 Elsevier Inc. All rights reserved.
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