Role of calcium-activated potassium channels and cyclic nucleotides on pulmonary vasoreactivity to serotonin.
Role of calcium-activated potassium channels and cyclic nucleotides on pulmonary vasoreactivity to serotonin.
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钙激活钾通道和环核苷酸对肺血管血清素反应性的作用。
DOI：
10.1152/ajplung.1997.273.1.l142
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发表时间：
1997
期刊：
影响因子：
--
通讯作者：
Barman,SA
中科院分区：
文献类型：
--
作者：
Barman,SA
在离体犬肺血液灌注模型上，研究了Ca（2+）激活的K+通道调节和环核苷酸第二信使信号转导在犬肺血管对5-羟色胺反应中的作用。肺血管阻力和顺应性的测量采用血管闭塞技术。5-羟色胺（10（-5）M）通过降低大血管顺应性和中室顺应性，显著增加毛细血管前和毛细血管后阻力，显著降低总血管顺应性。四乙基铵离子（TEA+; 1 mM），一种Ca（2+）激活的K+通道抑制剂，能显著增强5-羟色胺对肺动脉和肺静脉的升压作用。用鸟苷3 '，5'-环一磷酸（cGMP）/腺苷3 '，5'-环一磷酸（cAMP）磷酸二酯酶抑制剂3-异丁基-1-甲基黄嘌呤（10（-5）M）、cAMP的细胞膜渗透性类似物二丁酰-cAMP（10（-5）M）或cAMP依赖性血管扩张剂异丙肾上腺素（10（-5）M）预处理可抑制动脉和静脉的肾上腺素能反应，而TEA+则相反。相比之下，cGMP的稳定膜渗透类似物8-溴-cGMP（10（-5）M）对5-羟色胺没有影响。这些结果表明，在犬肺血管中存在由Ca（2+）激活的K+通道活性介导的基础水平的血管舒张，并且这些K+通道的抑制增加肺血管张力并增强肺血管对5-羟色胺的反应。此外，这些数据表明cAMP诱导的肺血管舒张主要由Ca（2+）激活的K+通道介导，这些特异性K+通道的激活减弱了对5-羟色胺的升压反应。因此，cAMP第二信使系统与Ca（2+）激活的K+通道在犬肺血管反应性中存在着重要的联系。
The role of Ca(2+)-activated K+ channel modulation and cyclic nucleotide second messenger signal transduction in the canine pulmonary vascular response to serotonin was determined in the isolated blood-perfused dog lung. Pulmonary vascular resistances and compliances were measured using vascular occlusion techniques. Serotonin (10(-5) M) significantly increased precapillary and postcapillary resistance and significantly decreased total vascular compliance by decreasing large vessel compliance and middle compartment compliance. Tetraethylammonium ions (TEA+; 1 mM), an inhibitor of Ca(2+)-activated K+ channels, significantly potentiated the pressor effect to serotonin on both the pulmonary arteries and pulmonary veins. Pretreatment with the guanosine 3',5'-cyclic monophosphate (cGMP)/adenosine 3',5'-cyclic monophosphate (cAMP) phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (10(-5) M), the cell membrane-permeable analog of cAMP, dibutyryl-cAMP (10(-5) M), or the cAMP-dependent vasodilator isoproterenol (10(-5) M) inhibited the serotonergic response on both the arteries and veins, which was reversed by TEA+. In contrast, the stable membrane-permeable analog of cGMP, 8-bromo-cGMP (10(-5) M), had no effect on serotonin. These results indicate that there is a basal level of vasorelaxation in canine pulmonary blood vessels that is mediated by Ca(2+)-activated K+ channel activity and that inhibition of these K+ channels increases pulmonary vascular tone and potentiates the pulmonary vasoactive response to serotonin. Also, these data suggest that cAMP-induced pulmonary vasodilation is mediated primarily by Ca(2+)-activated K+ channels and that activation of these specific K+ channels attenuates the pressor response to serotonin. Thus an important relationship appears to exist between the cAMP second messenger system and Ca(2+)-activated K+ channels in canine pulmonary vasoreactivity.
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酮色林对离体灌注大鼠肺中血清素诱导的血管反应的影响。
影响因子：
5
作者：
M. Le Roux;J. Syce
通讯作者：
J. Syce
DOI：
10.1152/ajpcell.1993.265.1.c299
发表时间：
1993-07
期刊：
The American journal of physiology
影响因子：
--
作者：
B. E. Robertson;R. Schubert;Jorgen Hescheler;M. Nelson
通讯作者：
B. E. Robertson;R. Schubert;Jorgen Hescheler;M. Nelson
影响因子：
20.1
作者：
LEE, SL;WANG, WW;FANBURG, BL
通讯作者：
FANBURG, BL
肺血管床中腺苷和ATP的信号转导机制。
DOI：
10.1152/ajpheart.1992.262.3.h926
发表时间：
1992
期刊：
The American journal of physiology
影响因子：
--
作者：
Lippton,HL;Hao,Q;Hauth,T;Hyman,A
通讯作者：
Hyman,A
TEA 抑制 ACh 诱导的 EDRF 释放：内皮 Ca(2) 依赖性 K 通道有助于血管张力。
DOI：
10.1152/ajpheart.1994.267.3.h1135
发表时间：
1994
期刊：
The American journal of physiology
影响因子：
--
作者：
Demirel,E;Rusko,J;Laskey,RE;Adams,DJ;vanBreemen,C
通讯作者：
vanBreemen,C