ATP-sensitive K+ (KATP) channels contribute to exercise-induced hyperemia in skeletal muscle either locally by vascular hyperpolarization or by sympathoinhibition and decreased sympathetic vasoconstriction. However, mean arterial pressure (MAP) regulation via baroreceptors and subsequent efferent activity may confound assessment of vascular versus neural KATP channel function. We hypothesized that systemic KATP channel inhibition via glibenclamide (GLI) would increase MAP without increasing sympathetic nerve discharge (SND). Lumbar and renal nerve SND were measured in anesthetized male rats with intact baroreceptors (n = 12) and sinoaortic denervated (SAD; n = 4) counterparts and blood flow (BF) and vascular conductance (VC) assessed in conscious rats (n = 6). GLI increased MAP (p < 0.05) and transiently decreased HR in intact (p < 0.05), but not SAD rats. Renal (-30 %) and lumbar (-40 %) ΔSND decreased in intact but increased in SAD rats (∼40 % and 20 %; p < 0.05). BF and VC decreased in kidneys and total hindlimb skeletal muscle (p < 0.05). Thus, because KATP inhibition decreases SND, GLI-induced reductions in blood flow cannot result from enhanced sympathetic activity.

中文翻译：

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在大鼠中抑制 ATP 敏感的 K+ 通道会减少肾脏和骨骼肌血流量，而不会增加交感神经放电。

ATP 敏感的 K+ (KATP) 通道通过局部血管超极化或交感神经抑制和交感神经血管收缩减少导致骨骼肌运动引起的充血。然而，通过压力感受器和随后的传出活动调节平均动脉压 (MAP) 可能会混淆血管与神经 KATP 通道功能的评估。我们假设通过格列本脲 (GLI) 的全身 KATP 通道抑制会增加 MAP 而不会增加交感神经放电 (SND)。在具有完整压力感受器（n = 12）和窦主动脉去神经支配（SAD；n = 4）对应物的麻醉雄性大鼠中测量腰神经和肾神经 SND，并在清醒大鼠（n = 6）中评估血流量（BF）和血管电导（VC） ）。GLI 增加 MAP (p < 0.05) 并暂时降低完整的 HR (p < 0.05)，但不是 SAD 大鼠。肾 (-30 %) 和腰椎 (-40 %) ΔSND 在完整的情况下降低，但在 SAD 大鼠中增加（~40% 和 20%；p < 0.05）。BF 和 VC 在肾脏和总后肢骨骼肌中降低 (p < 0.05)。因此，因为抑制 KATP 会降低 SND，所以 GLI 引起的血流量减少不能由增强的交感神经活动引起。