Exercise Training Modulates the Effects of Lipoproteins on Acetylcholine-Induced Endothelial Calcium Signaling in Rat Aortas

Author:

Chen Hsiun-ing1,Kao Sheau-Li1,Tsai Ming-Ho1,Shiao Ming-Shi1,Jen Chauying Jack1

Affiliation:

1. Department of Physiology, College of Medicine, National Cheng Kung University, Tainan 701, Taiwan, Republic of China; and Department of Medical Research and Education, Veterans General Hospital, Taipei 112, Taiwan, Republic of China

Abstract

Exercise training improves vascular endothelial functions, while oxidized low-density lipoproteins (oxLDLs) impede them. We proposed that exercise training might influence the endothelial sensitivity to lipoprotein-induced vascular changes. Male Wistar rats either exercised on a leveled treadmill for 8 weeks or remained sedentary as the control. The endothelial intracellular calcium level (EC [Ca2+]i) in vitro was examined using dissected aortic segments treated with different lipoproteins, including native low-density lipoprotein (nLDL), various oxLDLs, and high-density lipoprotein (HDL). Our results indicated that i) none of the various lipoproteins directly evoked EC [Ca2+]i elevation; ii) the acetylcholine-evoked EC [Ca2+]i elevation in the control group was increased by nLDL and progressively suppressed by oxLDLs with increasing degrees of oxidation; iii) exercise training ameliorated the oxLDL-induced suppressive effects on acetylcholine-evoked EC [Ca2+]i elevation; iv) HDL potentiated the acetylcholine-evoked EC [Ca2+]i elevation in vessel segments from exercised rats but not those from control rats; and v) when HDL was present, the suppressive effects of extensively modified oxLDLs were reduced. Furthermore, comparing with the effects of various lipoproteins on EC calcium signaling, the lipoprotein effects on endothelium-dependent vasorelaxing response appeared to be similar but less pronounced. Taken together, one of the beneficial effects of exercise training on vascular functions might be to make blood vessels more resistant to oxLDLs and more sensitive to HDL.

Publisher

SAGE Publications

Subject

General Biochemistry, Genetics and Molecular Biology

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