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首页> 外文期刊>Life sciences >INHIBITION OF CGMP MEDIATED RELAXATION IN SMALL RAT CORONARY ARTERIES BY BLOCK OF CA++ ACTIVATED K+ CHANNELS
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INHIBITION OF CGMP MEDIATED RELAXATION IN SMALL RAT CORONARY ARTERIES BY BLOCK OF CA++ ACTIVATED K+ CHANNELS

机译：CA ++活化的K +通道阻滞CGMP介导的松弛在小大鼠冠状动脉中的作用

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The functional importance of Ca++ activated K+ (K-Ca) channels in cGMP mediated relaxation ofpressurized septal arteries (internal basal diameter 213 +/- 4 mu m) was investigated. Vascular tone was increased by the thromboxane A(2) analogue, U46619 and internal pressure was maintained at 60 mmHg. Vessels were tested with an endothelium independent agonist (nitroprusside) and endothelium dependent agonist (acetylcholine) of nitric oxide which activates soluble guanylate cydase. Receptor activation of particulate guanylate cyclase was tested by atrial natriuretic peptide. Direct changes in intracellular cGMP concentration were done with the cell permeable analog, 8-Bromo-cGMP. Tetraethylammonium ion (TEA(+)), 1 mM, significantly inhibited relaxation to nitroprusside from 10(-7) to 10(-3)M with a maximal inhibition of 53 +/- 8% at 10(-3)M. Relaxation to acetylcholine from 10(-9)M to 10(-5)M was significantly inhibited by TEA(+) with a maximal inhibition of 52 +/- 13% at 10(-7)M. TEA(+) significantly inhibited relaxation to 8-Bromo-cGMP from 10(-6)M to 10(-3)M with a maximal inhibition of 59 +/- 14% at 10(-4)M. The relaxation response to atrial natriuretic peptide from 10(-12)M to 10(-7)M was significantly inhibited by TEA(+) with a maximal inhibition of 84 +/- 5% at 10(-11)M. The large conductance K-Ca channel blocker, iberiotoxin, eliminated the relaxation response to 8-Bromo-cGMP (10(-3)M). The results suggest that a large portion of the dilator action of cGMP is mediated by effects on K+ membrane channels. [References: 29]
机译：研究了Ca ++激活的K +（K-Ca）通道在cGMP介导的间隔中动脉舒张（内部基底直径213 +/- 4μm）中的功能重要性。血栓烷A（2）类似物U46619可增加血管张力，内部压力维持在60 mmHg。用活化可溶鸟苷酸胞苷酶的一氧化氮的内皮依赖性激动剂（硝普钠）和内皮依赖性激动剂（乙酰胆碱）测试血管。心房利钠肽测试颗粒鸟苷酸环化酶的受体活化。细胞内cGMP浓度的直接变化是通过细胞可渗透的类似物8-Bromo-cGMP完成的。四乙铵离子（TEA（+））1 mM显着抑制了硝普钠从10（-7）到10（-3）M的松弛，在10（-3）M时最大抑制53 +/- 8％。从TEA（+）显着抑制从10（-9）M到10（-5）M乙酰胆碱的松弛，在10（-7）M时最大抑制52 +/- 13％。 TEA（+）显着抑制了从10（-6）M到10（-3）M到8-Bromo-cGMP的松弛，在10（-4）M时最大抑制了59 +/- 14％。从10（-12）M到10（-7）M对心钠素的舒张反应被TEA（+）显着抑制，在10（-11）M时最大抑制84 +/- 5％。大电导的K-Ca通道阻滞剂埃博毒素，消除了对8-Bromo-cGMP（10（-3）M）的松弛反应。结果表明，cGMP的大部分扩张作用是由对K +膜通道的影响介导的。 [参考：29]

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