Voltage-gated potassium channels and NOS contribute to a sustained cutaneous vasodilation elicited by local heating in an interactive manner in young adults
Voltage-gated potassium channels and NOS contribute to a sustained cutaneous vasodilation elicited by local heating in an interactive manner in young adults
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DOI：
10.1016/j.mvr.2017.12.001
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发表时间：
2018-05-01
影响因子：
3.1
通讯作者：
Kenny, Glen P.
中科院分区：
文献类型：
--
作者：
Fujii, Naoto;Halili, Lyra;Kenny, Glen P.
局部皮肤加热至42℃导致皮肤灌注迅速增加（初始峰值），随后是短暂的最低点和随后的持续升高（平台）。一些研究表明，一氧化氮合酶（NOS）在局部加热期间的高原反应中起着重要作用。在这项研究中，我们验证了电压门控钾（Kv）通道通过nos依赖机制在局部加热过程中促进皮肤血管舒张平台的假设。11名年轻男性（25 +/- 4岁）参与了这项研究，在四个皮内微透析部位测量皮肤血管传导（CVC），连续灌注1)乳酸林格氏（对照），2)10 mM氨基吡啶（Kv通道阻滞剂），3)10 mM N ω -硝基- l -精氨酸（NOS抑制剂），或4)4-氨基吡啶和N ω -硝基- l -精氨酸的组合。与对照组相比，单独抑制Kv通道减弱了在局部加热期间测量的初始峰值、最低点和平台阶段观察到的CVC的增加；相比之下，单独抑制NOS仅在最低点和平台期减弱CVC的增加（例如，平台反应：控制位点：59 +/- 5%最大值，Kv通道阻断位点：49 +/- 8%最大值，NOS抑制位点：35 +/- 11%最大值，联合抑制位点：40 +/- 12%最大值）。此外，当同时去除NOS的调制影响时，在局部加热响应的任何阶段，没有测量到Kv通道阻塞对CVC的影响。我们发现Kv通道和NOS以相互作用的方式促进局部加热介导的皮肤血管舒张持续增加（即平台期）。(243/250的话)。
Local skin heating to 42 degrees C causes rapid increases in cutaneous perfusion (initial peak), followed by a brief nadir and subsequent sustained elevation (plateau). Several studies have demonstrated that nitric oxide synthase (NOS) largely contributes to the plateau response during local heating. In this study, we tested the hypothesis that voltage-gated potassium (Kv) channels contribute to the plateau of the cutaneous vasodilation during local heating through NOS-dependent mechanisms. Eleven young males (25 +/- 4 years) participated in this study wherein cutaneous vascular conductance (CVC) was measured at four intradermal microdialysis sites that were continuously perfused with either 1) lactated Ringer (Control), 2) 10 mM-aminopyridine (Kv channel blocker), 3) 10 mM N omega-Nitro-L-arginine (NOS inhibitor), or 4) a combination of 4-aminopyridine and N omega-Nitro-L-arginine. In comparison to the Control site, the inhibition of Kv channels alone attenuated the increase in CVC observed at the initial peak, nadir, and plateau phases measured during local heating; in contrast, the inhibition of NOS alone attenuated the increase in CVC at the nadir and plateau phases only (e.g., plateau response: Control site: 59 +/- 5%max, Kv channel blockade site: 49 +/- 8%max, NOS inhibition site: 35 +/- 11%max, combined inhibition site: 40 +/- 12%max). Further, no effect of Kv channel blockade on CVC was measured at any phase of the local heating response when the modulating influence of NOS was simultaneously removed. We show that Kv channels and NOS contribute to the local heating mediated sustained increase (i.e., plateau) in cutaneous vasodilation in an interactive manner. (243/250 words).