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首页> 外文期刊>American Journal of Physiology >Blood pressure regulates the activity and function of the Na-K-2Cl cotransporter in vascular smooth muscle.
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Blood pressure regulates the activity and function of the Na-K-2Cl cotransporter in vascular smooth muscle.

机译：血压调节血管平滑肌中Na-K-2Cl共转运蛋白的活性和功能。

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The Na-K-2Cl cotransporter (NKCC1) is one of several transporters that have been linked to hypertension, and its inhibition reduces vascular smooth muscle tone and blood pressure. NKCC1 in the rat aorta is stimulated by vasoconstrictors and inhibited by nitrovasodilators, and this is linked to the contractile state of the smooth muscle. To determine whether blood pressure also regulates NKCC1, we examined the acute effect of hypertension on NKCC1 in rats after aortic coarctation. In the hypertensive aorta (28-mmHg rise in mean blood pressure), an increase in NKCC1 activity (measured as bumetanide-sensitive (86)Rb efflux) was apparent by 16 h and reached a plateau of 62% greater than control at 48 h. In contrast, there was a slight decrease in NKCC1 activity in the hypotensive aorta (21% decrease in mean blood pressure). Measurement of NKCC1 mRNA by real-time PCR revealed a fivefold increase in the hypertensive aorta compared with the hypotensive aorta or sham aorta. The inhibition by bumetanide of isometric force response to phenylephrine was significantly greater in the hypertensive aorta than in the control aorta or hypotensive aorta. We conclude that NKCC1 in rat aortic smooth muscle is regulated by blood pressure, most likely through changes in transporter abundance. This upregulation of NKCC1 is associated with a greater contribution to force generation in the hypertensive aorta. This is the first demonstration that NKCC1 in vascular smooth muscle is regulated by blood pressure and indicates that this transporter is important in the acute response of vascular smooth muscle to hypertension.
机译：Na-K-2Cl协同转运蛋白（NKCC1）是与高血压有关的几种转运蛋白之一，其抑制作用可降低血管平滑肌张力和血压。大鼠主动脉中的NKCC1被血管收缩剂刺激，并被硝基血管扩张剂抑制，这与平滑肌的收缩状态有关。为了确定血压是否也调节NKCC1，我们检查了主动脉缩窄后高血压对NKCC1的急性影响。在高血压主动脉（平均血压升高28 mmHg）中，NKCC1活性（以布美他尼敏感型（86）Rb外流测量）在16 h时明显升高，并在48 h达到了平稳状态的62％ 。相反，降压主动脉中NKCC1活性略有下降（平均血压下降21％）。通过实时PCR测量NKCC1 mRNA显示，与降压主动脉或假主动脉相比，高血压主动脉增加了五倍。布美他尼对苯氧肾上腺素的等轴测力反应的抑制作用在高血压主动脉中比在对照主动脉或低血压主动脉中明显更大。我们得出的结论是，大鼠主动脉平滑肌中的NKCC1受血压调节，很可能是通过转运蛋白丰度的变化来调节的。 NKCC1的这种上调与高血压主动脉中力产生的更大贡献有关。这是血管平滑肌中NKCC1受血压调节的第一个证明，表明该转运蛋白在血管平滑肌对高血压的急性反应中很重要。

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