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首页> 外文期刊>American Journal of Physiology >Pharmacological stimulation of soluble guanylate cyclase modulates hypoxia-inducible factor-1alpha in rat heart.
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Pharmacological stimulation of soluble guanylate cyclase modulates hypoxia-inducible factor-1alpha in rat heart.

机译：药理学上刺激可溶性鸟苷酸环化酶可调节大鼠心脏缺氧诱导因子-1α。

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摘要

Mechanical load and ischemia induce a series of adaptive physiological responses by activating the expression of O(2)-regulated genes, such as hypoxia inducible factor-1alpha (HIF-1alpha). The aim of this study was to explore the interaction between HIF-1alpha and soluble guanylate cyclase (sGC) and its second messenger cGMP in cultured cardiomyocytes exposed to hypoxia and in pressure-overloaded heart. In cultured cardiomyocytes of neonatal rats, either sGC stimulator BAY 41-2272 or cGMP analog 8-bromo-cGMP decreased the hypoxia (1% O(2)/5% CO(2))-induced HIF-1alpha expression, whereas the inhibition of protein kinase G by KT-5823 reversed the effect of BAY 41-2272 on the expression under hypoxic conditions. In pressure-overloaded heart induced by suprarenal aortic constriction (AC) in 7-wk-old male Wistar rats, the administration of BAY 41-2272 (2 mg.kg(-1).day(-1)) for 14 days significantly suppressed the protein expression of HIF-1alpha (P < 0.05), vascular endothelial growth factor (P < 0.01), and the number of capillary vessels (P < 0.01) induced by pressure overload. This study suggests that the pharmacological sGC-cGMP stimulation modulates the HIF-1alpha expression in response to hypoxia or mechanical load in the heart.
机译：机械负荷和局部缺血通过激活O（2）调控的基因，如缺氧诱导因子1α（HIF-1alpha）的表达，诱导一系列适应性生理反应。这项研究的目的是探讨暴露于缺氧和压力超负荷的心肌细胞中HIF-1α与可溶性鸟苷酸环化酶（sGC）及其第二信使cGMP之间的相互作用。在新生大鼠的培养的心肌细胞中，sGC刺激物BAY 41-2272或cGMP类似物8-bromo-cGMP均可降低低氧（1％O（2）/ 5％CO（2））诱导的HIF-1alpha表达，而抑制在低氧条件下，KT-5823对蛋白激酶G的抑制逆转了BAY 41-2272对表达的影响。在7周龄雄性Wistar大鼠的肾上主动脉缩窄（AC）引起的压力超负荷的心脏中，BAY 41-2272（2 mg.kg（-1）.day（-1））的给药显着延长了14天抑制压力超负荷诱导的HIF-1α蛋白表达（P <0.05），血管内皮生长因子（P <0.01）和毛细血管数量（P <0.01）。这项研究表明，药理学sGC-cGMP刺激可调节HIF-1alpha的表达，以响应心脏的缺氧或机械负荷。

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