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Aerobic exercise-induced inhibition of PKCα/CaV1.2 pathway enhances the vasodilation of mesenteric arteries in hypertension
Archives of Biochemistry and Biophysics ( IF 3.559 ) Pub Date : 2019-11-13 , DOI: 10.1016/j.abb.2019.108191
Yu Chen, Yanyan Zhang, Meiling Shan, Yang Zhou, Yanjun Huang, Lijun Shi

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 (CaV1.2) 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 CaV1.2 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 (CaV1.2 agonist) elicited vasoconstriction, while Gö6976 (PKCα inhibitor) and nifedipine (CaV1.2 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 CaV1.2 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 CaV1.2 α1C subunit in VSMCs. These data indicate that hypertension enhanced PKCα/CaV1.2 pathway-induced constriction of mesenteric arteries, and this pathological enhancement is inhibited by aerobic exercise training.
更新日期:2019-11-13

 

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