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首页> 外文期刊>Hypertension research: Official journal of the Japanese Society of Hypertension >Pressure-independent effects of pharmacological stimulation of soluble guanylate cyclase on fibrosis in pressure-overloaded rat heart.
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Pressure-independent effects of pharmacological stimulation of soluble guanylate cyclase on fibrosis in pressure-overloaded rat heart.

机译：药理学刺激可溶性鸟苷酸环化酶对压力超负荷大鼠心脏纤维化的压力非依赖性作用。

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摘要

Cardiac fibrosis is a hallmark of cardiovascular remodeling associated with hypertension. The purpose of this study was to explore the effect and mechanism of soluble guanylate cyclase (sGC) stimulator BAY 41-2272, leading to intracellular cyclic guanosine monophosphate (cGMP) elevation, on the remodeling process induced by pressure overload. Seven-week-old male Wistar rats with hypertension induced by suprarenal aortic constriction (AC) were treated orally with 2 mg kg(-1) day(-1) of BAY 41-2272 for 14 days. BAY 41-2272 had no effects on blood pressure, but decreased AC-induced collagen accumulation in the left ventricle (LV), inhibiting the number of myofibroblasts and gene expressions of transforming growth factor-beta1 and type 1 collagen. In addition, the antifibrotic action of BAY 41-2272 was accompanied by reducing AC-induced angiotensin-converting enzyme (ACE) mRNA and its enzymatic activity, and angiotensin II concentration in LV. In cultured cardiac fibroblasts, BAY 41-2272 inhibited ACE synthesis and myofibroblast transformation, accompanied by elevating the intracellular cGMP concentration. These results suggest that sGC stimulator BAY 41-2272 might be effective to reduce fibrosis in hypertensive heart disease by attenuating angiotensin II generation through myofibroblast transformation.Hypertension Research (2009) 32, 597-603; doi:10.1038/hr.2009.64; published online 8 May 2009.
机译：心脏纤维化是与高血压相关的心血管重塑的标志。这项研究的目的是探讨可溶性鸟苷酸环化酶（sGC）刺激物BAY 41-2272导致细胞内环鸟苷单磷酸（cGMP）升高的作用及其机制，此过程是压力超负荷引起的。用2 mg kg（-1）day（-1）的BAY 41-2272口服治疗七周大的雄性Wistar大鼠，由肾上动脉主动脉缩窄（AC）诱发高血压，持续14天。 BAY 41-2272对血压没有影响，但减少了AC诱导的左心室（LV）引起的胶原蛋白积聚，从而抑制了肌成纤维细胞的数量以及转化生长因子β1和1型胶原蛋白的基因表达。此外，BAY 41-2272的抗纤维化作用伴随着AC诱导的血管紧张素转换酶（ACE）mRNA及其酶活性的降低，以及LV中血管紧张素II浓度的降低。在培养的心脏成纤维细胞中，BAY 41-2272抑制ACE合成和成纤维细胞转化，并伴有细胞内cGMP浓度升高。这些结果表明，sGC刺激物BAY 41-2272可能通过减弱通过成肌纤维细胞转化的血管紧张素II的产生来有效减少高血压性心脏病的纤维化。HypertensionResearch（2009）32，597-603; doi：10.1038 / hr.2009.64; 2009年5月8日在线发布。

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