Regular exercise is regarded as a nonpharmacological therapy for controlling hypertension by improving the function of vascular smooth muscle cells (VSMCs). The underlying mechanism is unclear. L-type-voltage-dependent Ca²⁺ channel (Ca_V1.2) on the plasma membrane and PKCα of VSMCs are pivotal modulators of vascular tone. PKCα is hyperactivated and concentrated at the surface membrane during hypertension. This study investigated the effects of aerobic exercise on the PKCα and Ca_V1.2 in mesenteric arterial smooth muscle cells from spontaneously hypertensive rats (SHRs). SHRs and Wistar-Kyoto (WKY) rats were randomly assigned into sedentary groups (SHR-SED and WKY-SED) and exercise training groups (SHR-EX and WKY-EX). Exercise groups were performed a 12-week moderate-intensity (18–20 m/min) treadmill training. Mesenteric arterial mechanical and functional properties were evaluated. Exercise reduced body weight and systolic blood pressure in both SHR-EX and WKY-EX. PDBu (PKC activator) and BayK 8644 (Ca_V1.2 agonist) elicited vasoconstriction, while Gö6976 (PKCα inhibitor) and nifedipine (Ca_V1.2 blocker) induced vasodilation of the vessel rings. In SHRs, exercise normalized the increased vascular sensitivity to these activators and inhibitors. Nifedipine greatly suppressed PDBu-induced vasoconstriction. Upon incubation with Gö6976, the effects of both PDBu and nifedipine were markedly suppressed. In patch-clamp studies, PDBu increased and Gö6976 decreased the Ca_V1.2 current density. Exercise ameliorated the responses of both PDBu and Gö6976 in SHRs. Immunofluorescence staining suggested that exercise training alleviated the hypertension-induced increase of colocalization rate of PKCα and Ca_V1.2 α_1C subunit in VSMCs. These data indicate that hypertension enhanced PKCα/Ca_V1.2 pathway-induced constriction of mesenteric arteries, and this pathological enhancement is inhibited by aerobic exercise training.

定期运动被认为是通过改善血管平滑肌细胞（VSMC）的功能来控制高血压的非药物疗法。潜在的机制尚不清楚。质膜上的L型电压依赖性Ca ²⁺通道（Ca _V 1.2）和VSMC的PKCα是血管张力的关键调节剂。高血压期间，PKCα过度活化并聚集在表膜上。这项研究调查了有氧运动对PKCα和Ca _V的影响1.2来自自发性高血压大鼠（SHRs）的肠系膜动脉平滑肌细胞。将SHR和Wistar-Kyoto（WKY）大鼠随机分为久坐组（SHR-SED和WKY-SED）和运动训练组（SHR-EX和WKY-EX）。运动组进行了为期12周的中等强度（18–20 m / min）跑步机训练。评估肠系膜动脉的机械和功能特性。在SHR-EX和WKY-EX中，运动均可减轻体重和收缩压。PDBu（PKC激活剂）和BayK 8644（Ca _V 1.2激动剂）引起血管收缩，而Gö6976（PKCα抑制剂）和硝苯地平（Ca _V1.2阻滞剂）引起血管环的血管舒张。在SHR中，运动使对这些激活剂和抑制剂的血管敏感性正常化。硝苯地平极大地抑制了PDBu引起的血管收缩。与Gö6976一起孵育后，PDBu和硝苯地平的作用均被显着抑制。在膜片钳研究中，PDBu升高，Gö6976降低Ca _V 1.2电流密度。锻炼改善了SHR中PDBu和Gö6976的反应。免疫荧光染色表明，运动训练缓解PKCα和Ca的共定位速率的高血压引起的增加_V 1.2α _1C在血管平滑肌细胞亚基。这些数据表明高血压增强了PKCα/ Ca _V1.2途径引起的肠系膜动脉收缩，这种病理性增强受到有氧运动训练的抑制。