No independent, but an interactive, role of calcium-activated potassium channels in human cutaneous active vasodilation.

No independent, but an interactive, role of calcium-activated potassium channels in human cutaneous active vasodilation.
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钙激活钾通道在人体皮肤主动血管舒张中没有独立的作用,而是相互作用的。

DOI:
10.1152/japplphysiol.00358.2013
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发表时间:
2013
期刊:
Journal of applied physiology (Bethesda, Md. : 1985)
影响因子:
--
通讯作者:
Minson,ChristopherT
Minson,ChristopherT
中科院分区:
--
文献类型:
--
作者:
Brunt,ViennaE;Fujii,Naoto;Minson,ChristopherT

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在人体皮肤微血管中,内皮源性超极化因子(EDHFs)在与局部刺激相关的血管舒张中占很大一部分。因此,我们试图确定edhf在主动血管舒张(AVD)被动加热两种方案中的作用。采用水灌注服实现全身加热(核心温度升高0.8 ~ 1.0℃),采用激光多普勒血流仪测量皮肤血流量。在第一种方案中,四个部位通过微透析连续灌注,1)对照;2)四乙基铵(TEA)阻断钙活化钾(KCa)通道,从而影响EDHFs的作用;3) n -硝基精氨酸甲酯(l-NAME)抑制一氧化氮合酶(NOS);4) TEA +l-NAME (n= 8)。数据以最大皮肤血管传导率(CVC)百分比表示。TEA对AVD没有影响(加热平台期CVC:对照组57.4±4.9% vs TEA 63.2±5.2%,P= 0.27),表明edhf不是强制性的。l-NAME使高原CVC降至33.7±5.4% (P< 0.01);而TEA +l-NAME组与单独使用l-NAME组相比,可提高高原CVC(49.7±5.3%,P= 0.02)。从这些数据来看,EDHFs和NOS的联合阻断需要通过其他方式进行扩张,可能通过内向整流(KIR)和/或atp敏感(KATP)钾通道。为了验证第二个假设,我们测量了以下位点(n= 8)的AVD:1)对照,2)l-NAME,3)l-NAME + TEA, 4)l-NAME + TEA +氯化钡(BaCl2; KIRand KATPblocker)。加入bacl2tel - name + TEA可使高原CVC降低至32.7±6.6% (P= 0.02 vs.l-NAME + TEA),与el- name组无差异。这些数据表明血管舒张通路之间存在复杂的相互作用,存在NO、kcachanchannels和KIRand/或KATPchannels之间的串扰。
In human cutaneous microvasculature, endothelium-derived hyperpolarizing factors (EDHFs) account for a large portion of vasodilation associated with local stimuli. Thus we sought to determine the role of EDHFs in active vasodilation (AVD) to passive heating in two protocols. Whole body heating was achieved using water-perfused suits (core temperature increase of 0.8–1.0°C), and skin blood flow was measured using laser-Doppler flowmetry. In the first protocol, four sites were perfused continuously via microdialysis with:1) control;2) tetraethylammonium (TEA) to block calcium-activated potassium (KCa) channels, and thus the actions of EDHFs;3)N-nitro-l-arginine methyl ester (l-NAME) to inhibit nitric oxide synthase (NOS); and4) TEA +l-NAME (n= 8). Data are presented as percent maximal cutaneous vascular conductance (CVC). TEA had no effect on AVD (CVC during heated plateau: control 57.4 ± 4.9% vs. TEA 63.2 ± 5.2%,P= 0.27), indicating EDHFs are not obligatory.l-NAME attenuated plateau CVC to 33.7 ± 5.4% (P< 0.01 vs. control); while TEA +l-NAME augmented plateau CVC compared withl-NAME alone (49.7 ± 5.3%,P= 0.02). From these data, it appears combined blockade of EDHFs and NOS necessitates dilation through other means, possibly through inward rectifier (KIR) and/or ATP-sensitive (KATP) potassium channels. To test this second hypothesis, we measured AVD at the following sites (n= 8):1) control,2)l-NAME,3)l-NAME + TEA, and4)l-NAME + TEA + barium chloride (BaCl2; KIRand KATPblocker). The addition of BaCl2tol-NAME + TEA reduced plateau CVC to 32.7 ± 6.6% (P= 0.02 vs.l-NAME + TEA), which did not differ from thel-NAME site. These data combined demonstrate a complex interplay between vasodilatory pathways, with cross-talk between NO, KCachannels, and KIRand/or KATPchannels.
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