Mechanisms of anesthetics on in situ normotensive vs hypertensive rat mesenteric vascular smooth muscle transmembrane potentials

由于血管平滑肌（VSM）跨膜电位（Em）与活跃的VSM张力之间存在紧密的线性耦合，这种超极化反映了血管松弛。在基础麻醉下的正常和高血压大鼠中，我们通过剖腹中线外化一个包含肠系膜动脉和静脉的空肠袢，并将其灌注生理盐溶液。用玻璃微电极记录原位肠系膜阻抗（动脉）和电容（静脉）血管（6-羟多巴胺）去神经支配或不去神经支配。在血压正常的大鼠中，吸入麻醉剂（异氟醚、七氟醚）和氯胺酮在肠系膜动脉和静脉均呈高极化。吸入麻醉剂减弱了交感神经和非神经对VSM跨膜电位（和张力）的调节。高血压大鼠吸入麻醉剂超极化比正常大鼠更负。在血管制剂的过浓液中（在血压正常的大鼠中）施用已知存在于VSM中的四种钾通道的选择性抑制剂，以评估其对异氟烷介导的超极化的影响。异氟醚介导的VSM的超极化可以部分归因于钙激活的和三磷酸腺苷敏感的钾通道的增强（或维持）开放，而不是电压依赖性的或内向整流的钾通道。

Since tight linear coupling exists between vascular smooth muscle (VSM) transmembrane potential (Em) and active VSM tone, such hyperpolarization reflects a vasorelaxation.In normotensive and hypertensive rats under basal anesthesia, we externalized a loop of jejunum containing mesenteric arteries and veins through a midline laparotomy and superfused them with physiological salt solution. Ems were recorded from in situ mesenteric resistance (arteries) and capacitance (veins) vessels with or without denervation (by 6- hydroxydopamine) using glass microelectrode. In normotensive rats, inhaled anesthetics (isoflurane, sevoflurane) and ketamine hyperpolarized in both mesenteric arteries and veins. Inhaled anesthetics attenuated both sympathetic neural and nonneural regulation of VSM transmembrane potentials ( and tone). Inhaled anesthetics hyperpolarized in hypertensive rats more negative than in normotensive rats.Selective inhibitors of each of four types of potassium channels known to exist in VSM were administered in superfusate of the vessel preparations (in normotensive rats) to assess their effects on isoflurane-mediated hyperpolarization. Isoflurane-mediated hyperpolarization of VSM can be attributed in part to an enhanced (or maintained) opening of calcium-activated and adenosine triphosphate sensitive potassium channels but not voltage-dependent or inward rectifier potassium channels.