Saturday, December 17, 2016

Aerobic exercise of low to moderate intensity corrects unequal changes in BK(Ca)-subunit expression in the mesenteric arteries of spontaneously hypertensive rats.

Aerobic exercise of low to moderate intensity corrects unequal changes in BK(Ca)-subunit expression in the mesenteric arteries of spontaneously hypertensive rats.

Physiol Res. 2016 Dec 16;

Authors: Zhang Y, Chen Y, Zhang L, Lu N, Shi L


Accumulating evidence indicates that hypertension is associated with "ion channel remodeling" of vascular smooth muscle cells (VSMCs). The objective of this study was to determine the effects of exercise intensity/volume on hypertension-associated changes in large-conductance Ca(2+)-activated K(+) (BK(Ca)) channels in mesenteric arteries (MAs) from spontaneously hypertensive rats (SHR). Male SHRs were randomly assigned to three groups: a low-intensity aerobic exercise group (SHR-L: 14 m/min), a moderate-intensity aerobic exercise group (SHR-M: 20 m/min), and a sedentary group (SHR). Age-matched Wistar-Kyoto rats (WKYs) were used as normotensive controls. Exercise groups completed an 8-week exercise program. Elevation of the alpha and beta1 proteins was unequal in MA myocytes from SHRs, with the beta1-subunit increasing more than the alpha-subunit. BK(Ca) contribution to vascular tone regulation was higher in the myocytes and arteries of SHRs compared to WKYs. SHR BK(Ca) channel subunit protein expression, beta1/alpha ratio, whole cell current density and single-channel open probability was also increased compared with WKYs. Aerobic exercise lowered systemic blood pressure and normalized hypertension-associated BK(Ca) alterations to normotensive control levels in the SHRs. These effects were more pronounced in the moderate-intensity group than in the low-intensity group. There is a dose-effect for aerobic exercise training in the range of low to moderate-intensity and accompanying volume for the correction of the pathological adaptation of BK(Ca) channels in myocytes of MAs from SHR.

27982688

Read More