title: Exercise training reverses alterations in Kv and BKCa channel molecular expression in thoracic aorta smooth muscle cells from spontaneously hypertensive rats.
abstract: Previous studies have shown that exercise training influences potassium channel protein expression in arteries. The purpose of this study was to investigate the effect of exercise training on alterations in voltage-gated potassium channels (Kv) and large-conductance, calcium-activated potassium channels (BKCa) in thoracic aorta smooth muscle cells from spontaneously hypertensive rats (SHRs). Male SHRs were randomly assigned to a sedentary group (SHR-SED) and exercise training group (SHR-EX). Age-matched Wistar-Kyoto rats (WKYs) were used as controls. After 8 weeks of aerobic exercise training, blood pressure was significantly lower in the SHR-EX group than in the SHR-SED group. Exercise training increased the contribution of the Kv1.2 and Kv1.5 channels and decreased the contribution of BKCa channel to resting tone in the SHR-EX group compared to the SHR-SED group as indicated by vessel contractility experiments. Immunohistochemistry and Western blotting showed that Kv1.2 and Kv1.5 channel expression was significantly lower in the SHR-SED group than in the WKY group and exercise training attenuated this reduction. BKCa α-subunit expression was statistically unchanged between the groups; however, β1-subunit expression was reduced significantly by exercise training in the SHR-EX group compared to the SHR-SED group. These data suggest that exercise training reverses the pathological expression of the Kv1.2, Kv1.5, and BKCa channels in aortic myocytes from SHRs. This is one of the favorable effects of exercise training on large conduit arteries.
authors: Department of Exercise Physiology, Beijing Sport University, Beijing, China.
authors: Zhencheng
authors: Z
authors: Li
authors: Ni
authors: N
authors: Lu
authors: Lijun
authors: L
authors: Shi
mesh_terms: D000818:Animals; D001013:Aorta, Thoracic / Q000378:metabolism / Q000503:physiopathology; D001794:Blood Pressure; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D005081:Exercise Therapy; D006973:Hypertension / Q000378:metabolism / Q000503:physiopathology / Q000628:therapy*; D051663:Kv1.2 Potassium Channel / Q000037:antagonists & inhibitors / Q000378:metabolism*; D051666:Kv1.5 Potassium Channel / Q000037:antagonists & inhibitors / Q000378:metabolism*; D051037:Large-Conductance Calcium-Activated Potassium Channel alpha Subunits / Q000037:antagonists & inhibitors / Q000378:metabolism*; D008297:Male; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000378:metabolism* / Q000503:physiopathology; D032389:Myocytes, Smooth Muscle / Q000187:drug effects / Q000378:metabolism*; D005082:Physical Exertion; D026902:Potassium Channel Blockers / Q000494:pharmacology; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D013997:Time Factors; D014661:Vasoconstriction; D014662:Vasoconstrictor Agents / Q000494:pharmacology
chemical_list: C496972:Kcna2 protein, rat; C496983:Kcna5 protein, rat; C494842:Kcnma1 protein, rat; D051663:Kv1.2 Potassium Channel; D051666:Kv1.5 Potassium Channel; D051037:Large-Conductance Calcium-Activated Potassium Channel alpha Subunits; D026902:Potassium Channel Blockers; D014662:Vasoconstrictor Agents