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当心脏持续暴露在各种压力和损伤时,心脏发生重构。心肌纤维化是心脏重构的主要特征。心脏局部的炎症反应和肾素—血管紧张素—醛固酮系统的激活可促进心肌纤维化。在心肌纤维化的过程中,炎症因子如肿瘤坏死因子α、白细胞介素1和白细胞介素6等被激活,且这些炎症因子可加重心肌纤维化。脑钠尿肽是主要由心室分泌的一种由32个氨基酸构成的多肽。心室分泌的脑钠尿肽通过作用于其受体使得环磷酸鸟苷水平升高从而发挥其生物效应。脑钠尿肽具有调节肾血流量、扩张血管、抑制肾素—血管紧张素—醛固酮系统、抗纤维化及抗炎等多种作用。心力衰竭时,脑钠尿肽可以减轻心脏的前后负荷,减轻心脏重塑,而且脑钠尿肽可抑制心脏局部血管紧张素Ⅱ、肿瘤坏死因子α、白细胞介素1和白细胞介素6等引起的心脏纤维化。
When the heart continues to be exposed to various stresses and injuries, the heart is remodeled. Cardiac fibrosis is a major feature of cardiac remodeling. Local cardiac inflammatory response and renin-angiotensin-aldosterone system activation can promote myocardial fibrosis. In the process of myocardial fibrosis, inflammatory factors such as tumor necrosis factor alpha, interleukin-1 and interleukin-6 are activated, and these inflammatory cytokines can aggravate myocardial fibrosis. Brain natriuretic peptide is a 32 amino acid peptide secreted mainly by the ventricle. Ventricular secreted brain natriuretic peptide exerts its biological effect by acting on its receptor to raise the level of cyclic guanosine monophosphate. Brain natriuretic peptide can regulate renal blood flow, dilate blood vessels, inhibit renin - angiotensin - aldosterone system, anti-fibrosis and anti-inflammatory and other effects. In heart failure, BNP can relieve the heart anteroposterior load and relieve heart remodeling, and BNP can inhibit cardiac angiotensin Ⅱ, tumor necrosis factor α, interleukin-1 and interleukin-6 Heart fibrosis.