[A MODULATORY INFLUENCE OF THE iNOS ON THE FUNCTIONAL ACTIVITY OF THE KATP-CHANNELS IN CORONARY VESSELS OF RATS ADAPTED TO THE STRESS].

S S Lazuko, L E Belyaeva, E B Manuchina
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Abstract

In the experiments carried out on the isolated by Langendorff's method hearts which were perfused at the constant coronary flow it was studied influence of iNOS-derived NO on the functional activity of the KATP-channels in the coronary vascular smooth muscle cells following formation of the adaptation to the stress. As an adaptation to the short stress as a 6-hours immobilization stress result in increase of NO production and rise of expression of gene iNOS; however, adaptation in contrast to the stress leads to moderate accumulation of iNOS against the background unchanged systemic activity of еNOS and in the absence of systemic low-grade inflammation. After an adaptation to the short stress or after 6 hours of immobilization the functional glybenclamid-inhibiting activity of the KATP-channels was suppressed. Nevertheless, after prolonged immobilization suppressed activity of the channels was abolished after blockage of iNOS, whereas iNOS blockage in adapted animals leads not only to the recovery but even to the hyperactivation of the KATP-channels. Hence, increase in NO production which is typical for the adaptation, limits activation of the KATP-channels thus creating a strong link between these channels activity and NO produced by iNOS.

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在适应应激的大鼠冠状血管中,iNOS对katp通道功能活性的调节作用。
在Langendorff法离体心脏恒冠状动脉血流灌注实验中,研究了应激适应形成后inos来源NO对冠状血管平滑肌细胞中katp通道功能活性的影响。作为对短应激的适应,6小时固定应激导致NO产量增加,基因iNOS表达升高;然而,与应激相比,适应性导致iNOS的适度积累,而背景是系统的nos活性不变,并且没有全身性低度炎症。在适应短应激或固定6小时后,katp通道的功能性格列本脲抑制活性被抑制。然而,在长时间固定后,抑制的通道活性在阻断iNOS后被消除,而在适应动物中,iNOS阻断不仅会导致katp通道的恢复,甚至会导致katp通道的过度激活。因此,适应过程中典型的NO产生的增加限制了katp通道的激活,从而在这些通道的活性和iNOS产生的NO之间建立了紧密的联系。
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