作者: Victor Kazanski , Andre Kamkin , Ekaterina Makarenko , Natalia Lysenko , Natalia Lapina
DOI: 10.1007/978-90-481-9881-8_5
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摘要: The article presents the effects of NO on myocardial functions including its pronounced influence myocardium contraction and heart rhythm. Attention is given to cell signaling nitric oxide in heart. It demonstrated that general final effect depends cellular source NO, amount release, prevailing redox balance antioxidant status, stimuli such as coronary flow rate rate, target tissue, interaction with neurohumoral other stimuli, activity level immune system activation cGMP-dependent independent intracellular cascades. A number experiments conducted whole hearts lets us suppose NO-synthases origins, directly regulate conductivity mechanically gated channels (MGCs). This study discusses experimental data obtained from isolated ventricular myocytes mouse, rat guinea pig by means patch-clamp whole-cell configuration about role regulation MGCs. Presented demonstrate donors lead MGCs appearance MG-like currents unstretched myocytes, while stretched cells activated inactivation inhibition these channels. scavenger PTIO causes all In conductance through blocked, which present control before deformation. complete stretch induced MG-current during presence stretch. Application non selective inhibitors L-NAME or L-NMMA resulted a blockade presented are instituted transgenic mice. wild-type mice, NOS1–/– NOS2–/– stretching results an typical MG-currents. On contrary, NOS3–/– mice does not activate suggest plays important cardiomyocytes NOS3 dominates origin.