Exercise training reverses alterations in Kv and BKCa channel molecular expression in thoracic aorta smooth muscle cells from spontaneously hypertensive rats
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Exercise training reverses alterations in Kv and BKCa channel molecular expression in thoracic aorta smooth muscle cells from spontaneously hypertensive rats. / Li, Zhencheng; Lu, Ni; Shi, Lijun.
In: Journal of Vascular Research, Vol. 51, No. 6, 2014, p. 447-457.Research output: Contribution to journal › Journal article › Research › peer-review
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TY - JOUR
T1 - Exercise training reverses alterations in Kv and BKCa channel molecular expression in thoracic aorta smooth muscle cells from spontaneously hypertensive rats
AU - Li, Zhencheng
AU - Lu, Ni
AU - Shi, Lijun
N1 - (Ekstern)
PY - 2014
Y1 - 2014
N2 - 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 (SHRSED) 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 Kv 1.2 and Kv 1.5 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 Kv 1.2 and Kv 1.5 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 Kv 1.2, Kv 1.5, and BKCa channels in aortic myocytes from SHRs. This is one of the favorable effects of exercise training on large conduit arteries.
AB - 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 (SHRSED) 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 Kv 1.2 and Kv 1.5 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 Kv 1.2 and Kv 1.5 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 Kv 1.2, Kv 1.5, and BKCa channels in aortic myocytes from SHRs. This is one of the favorable effects of exercise training on large conduit arteries.
KW - Faculty of Science
KW - Potassium channels
KW - Spontaneously hypertensive rat
KW - Exercise training
KW - Thoracic aorta
UR - http://europepmc.org/abstract/med/25661478
U2 - 10.1159/000369928
DO - 10.1159/000369928
M3 - Journal article
C2 - 25661478
VL - 51
SP - 447
EP - 457
JO - Journal of Vascular Research
JF - Journal of Vascular Research
SN - 1018-1172
IS - 6
ER -
ID: 273700187