title: Exercise intensity-dependent reverse and adverse remodeling of voltage-gated Ca(2+) channels in mesenteric arteries from spontaneously hypertensive rats.
abstract: Exercise can be regarded as a drug for treating hypertension, and the 'dosage' (intensity/volume) is therefore of great importance. L-type voltage-gated Ca(2+) (Cav1.2) channels on the plasma membrane of vascular smooth muscle cells have a pivotal role in modulating the vascular tone, and the upregulation of Cav1.2 channels is a hallmark feature of hypertension. The present study investigated the beneficial and adverse effects of exercise at different intensities on the remodeling of the Cav1.2 channel in mesenteric arteries (MAs) of spontaneously hypertensive rats (SHRs). Moderate- (SHR-M, 18-20 m min(-1)) and high-intensity (SHR-H, 26-28 m min(-1)) aerobic exercise training groups were created for SHRs and lasted for 8 weeks (1 h per day, 5 d per week). Age-matched sedentary SHRs and normotensive Wistar-Kyoto rats (WKY) were used as controls. The mesenteric arterial mechanical and functional properties were evaluated. Moderate-intensity exercise training induced a lower systolic blood pressure and heart rate in these rats compared with sedentary SHRs. BayK 8644 and nifedipine induced vasoconstriction and dose-dependent vasorelaxation, respectively, in the mesenteric arterial rings. Moderate-intensity exercise significantly suppressed the increase in BayK 8644-induced vasoconstriction, tissue sensitivity to nifedipine, Cav1.2 channel current density and Cav1.2 α1C-subunit protein expression in MAs from SHRs. However, high-intensity exercise training aggravated all of these hypertension-associated functional and molecular alterations of Cav1.2 channels. These results indicate that moderate-intensity aerobic training may act as a drug and effectively reverse the remodeling of Cav1.2 channels in hypertension to restore the vascular function in MAs, but that high-intensity exercise exaggerates the adverse remodeling of Cav1.2 channels and worsens the vascular function.
authors.affiliation: Department of Exercise Physiology, Beijing Sport University, Beijing, China.
authors.forename: Yu
authors.initials: Y
authors.lastname: Chen
authors.affiliation: Department of Exercise Physiology, Beijing Sport University, Beijing, China.
authors.forename: Hanmeng
authors.initials: H
authors.lastname: Zhang
authors.affiliation: Department of Exercise Physiology, Beijing Sport University, Beijing, China.
authors.forename: Yanyan
authors.initials: Y
authors.lastname: Zhang
authors.affiliation: Department of Exercise Physiology, Beijing Sport University, Beijing, China.
authors.forename: Ni
authors.initials: N
authors.lastname: Lu
authors.affiliation: Department of Exercise Physiology, Beijing Sport University, Beijing, China.
authors.forename: Lin
authors.initials: L
authors.lastname: Zhang
authors.affiliation: Department of Exercise Physiology, Beijing Sport University, Beijing, China.
authors.forename: Lijun
authors.initials: L
authors.lastname: Shi
mesh_terms: D000332:Aerobiosis; D000818:Animals; D001794:Blood Pressure; D002121:Calcium Channel Blockers / Q000494:pharmacology; D020746:Calcium Channels, L-Type / Q000378:metabolism*; D006339:Heart Rate; D008297:Male; D008638:Mesenteric Arteries / Q000378:metabolism*; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000378:metabolism; D009543:Nifedipine / Q000494:pharmacology; D005082:Physical Exertion; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D014665:Vasodilator Agents / Q000494:pharmacology
chemical_list: D002121:Calcium Channel Blockers; D020746:Calcium Channels, L-Type; C419385:L-type calcium channel alpha(1C); D014665:Vasodilator Agents; D009543:Nifedipine