The intracellular calcium regulation by the sodium diuretic peptide hormone in the impaired ventricular myocytes.

关于钠利尿肽激素（ANP、BNP、CNP）的心脏保护作用，已知钠诱导的利尿作用、血管扩张作用和对肾素-血管紧张素-醛固酮系统（RAAS）的抑制。衰竭心脏中RAAS的局部激活导致肌细胞肥大、纤维化、活性氧的产生以及RAAS的正反馈，最终产生醛固酮。ANP和BNP可能通过调节局部RAAS直接保护衰竭心肌。其保护机制可能主要是降低细胞内Ca^2+超载，包括（1）cGMP降低Ca^2+过量电流，（2）激活SR-Ca^2+泵，（3）与Na^+/Ca^2+交换体和/或Na^+/H^+交换体的相互作用。我们特别注意了ANP和BNP对心力衰竭或缺血/再灌注损伤时Na^+/Ca^<2+>交换和Na^+/H^+交换的保护作用。我们继续研究钠利尿肽激素对心肌细胞Ca^2+调节系统的影响，并探讨钠利尿肽激素在心力衰竭治疗策略中的可能应用。

As for the heart protective effects of sodium diuretic peptide hormones (ANP、BNP、CNP), the Na-induced diuretic effect, the vascular dilation effect, and the inhibition of the rennin-angiotensin-aldosterone system (RAAS) have been known. The local activation of RAAS in the failing heart leads to myocyte hypertrophy, fibrosis, production of reactive oxygen species, and positive feedback of RAAS with the final production of aldosterone. The possible regulation of local RAAS by ANP and BNP is expected to directly protect failing myocardium. The main mechanism of the protection may be the reduction of cellular Ca^<2+> overlolad, which includes (1)the reduction of the Ca^<2+> excess current by cyclic GMP, (2)the activation of the SR-Ca^<2+> pump, and (3)the interaction with Na^+/Ca^<2+> exchanger and/or Na^+/H^+ exchanger. We specially took notices of the protective effects of ANP and BNP on Na^+/Ca^<2+> exchanger and Na^+/H^+ exchanger in the failing heart or in the ischemic/reperfitsion injury. We continue to investigate the effects of sodium diuretic peptide hormones on the Ca^<2+> regulating system in cardiac myocytes with possible application of sodium diuretic peptide hormones to the therapeutic strategy in heart failure.