NO mediated activation of KATP channels contributes to cutaneous thermal hyperaemia in young adults.
NO mediated activation of KATP channels contributes to cutaneous thermal hyperaemia in young adults.
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NO 介导的 KATP 通道激活导致年轻人皮肤热充血。
DOI：
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发表时间：
2020
期刊：
影响因子：
--
通讯作者：
T. Nishiyasu
中科院分区：
文献类型：
--
作者：
Naoto Fujii;G. Mcgarr;G. Kenny;T. Amano;Y. Honda;N. Kondo;T. Nishiyasu
局部皮肤加热至42ºC主要通过一氧化氮合酶（NOS）相关机制引起皮肤热充血。我们评估了ATP敏感性K+（KATP）通道与NOS相互作用介导皮肤热充血的假设。在13名年轻人（6名女性）中，在4个皮内微透析部位测量皮肤血管传导性（CVC），这些部位连续灌注1）乳酸林格氏溶液（对照），2）5 mM格列本脲（KATP通道阻滞剂），3）20 mM N（G）-硝基-L-精氨酸甲酯（NOS抑制剂）或4）两者的组合。在所有四个治疗部位进行局部皮肤加热至42ºC，以引起皮肤热充血。局部加热后30分钟，将1.25 mM吡那地尔（Katp通道开放剂）和随后的25 mM硝普钠（NO供体）施用至4个部位中的3个（各25-30分钟）。格列本脲（19%）可减弱局部加热引起的CVC延长升高，但短暂的初始峰不减弱。然而，格列本脲在NOS抑制的情况下对CVC的长期升高没有影响。吡那地尔引起CVC升高，但在格列本脲处理的皮肤部位消除了这种反应，证明其作为KATP通道阻滞剂的有效性。吡那地尔诱导的CVC增加不受NOS抑制的影响，而硝普钠引起的CVC增加部分（15%）被格列本脲抑制。总之，我们发现KATP通道和NOS对皮肤热充血的平台有相互作用。这种相互作用可能反映了NO对血管平滑肌细胞KATP通道的激活。
Local skin heating to 42ºC causes cutaneous thermal hyperaemia largely via nitric oxide (NO) synthase (NOS) related mechanisms. We assessed the hypothesis that ATP-sensitive K+ (KATP) channels interact with NOS to mediate cutaneous thermal hyperaemia. In thirteen young adults (6 women), cutaneous vascular conductance (CVC) was measured at four intradermal microdialysis sites that were continuously perfused with either 1) lactated Ringer's solution (control), 2) 5 mM glibenclamide (KATP channel blocker), 3) 20mM N(G)-Nitro-L-arginine methyl ester (NOS inhibitor), or 4) a combination of both. Local skin heating to 42ºC was administered at all four treatment sites to elicit cutaneous thermal hyperaemia. Thirty minutes after the local heating, 1.25 mM pinacidil (KATP channel opener) and subsequently 25 mM sodium nitroprusside (NO donor) were administered to 3 of the 4 sites (each 25-30 min). The local-heating induced prolonged elevation in CVC was attenuated by glibenclamide (19%), but the transient initial peak was not. However, glibenclamide had no effect on the prolonged elevation in CVC in the presence of NOS inhibition. Pinacidil caused an elevation in CVC, but this response was abolished at the glibenclamide treated skin site, demonstrating its effectiveness as a KATP channel blocker. The pinacidil-induced increase in CVC was unaffected by NOS inhibition, whereas the increase in CVC elicited by sodium nitroprusside was partly (15%) inhibited by glibenclamide. In summary, we showed an interactive effect of KATP channels and NOS for the plateau of cutaneous thermal hyperaemia. This interplay may reflect a vascular smooth muscle cell KATP channel activation by NO.
皮肤神经元一氧化氮在体位性心动过速综合征中特别减少。
DOI：
10.1152/ajpheart.00600.2007
发表时间：
2007
期刊：
American journal of physiology. Heart and circulatory physiology
影响因子：
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作者：
Stewart,JulianM;Medow,MarvinS;Minson,ChristopherT;Taneja,Indu
通讯作者：
Taneja,Indu
影响因子：
3.3
作者：
Brunt, Vienna E.;Eymann, Taylor M.;Minson, Christopher T.
通讯作者：
Minson, Christopher T.