Key result
Physical activity maintained ACh-induced endothelium-dependent relaxation in OLETF rats from 13 to 40 weeks of age, potentially due to an increase in active aortic eNOS.
Why the study?
Does physical activity prevent the decline of ACh-induced endothelium-dependent relaxation in the obese type 2 diabetic OLETF rat?
Does physical activity prevent the decline of ACh-induced endothelium-dependent relaxation in the obese type 2 diabetic OLETF rat?
Physical activity maintains aortic endothelium-dependent relaxation in a rat model of type 2 diabetes, likely by increasing active aortic eNOS.
Answers are grounded in this paper and cite their sources.
May support exercise to preserve endothelial function in diabetic rat models; leaves open translation to human type 2 diabetes.
We tested the hypothesis that physical activity can attenuate the temporal decline of ACh-induced endothelium-dependent relaxation during type 2 diabetes mellitus progression in the Otsuka Long-Evans Tokushima fatty (OLETF) rat. Sedentary OLETF rats exhibited decreased ACh-induced abdominal aortic endothelium-dependent relaxation from 13 to 20 wk of age (20-35%) and from 13 to 40 wk of age (35-50%). ACh-induced endothelium-dependent relaxation was maintained in the physically active OLETF group and control sedentary Long-Evans Tokushima Otsuka (LETO) group from 13 to 40 wk of age. Aortic pretreatment with N(G)-nitro-l-arginine (l-NNA), indomethacin (Indo), and l-NNA + Indo did not alter the temporal decline in ACh-induced endothelium-dependent relaxation. Temporal changes in the protein expression of SOD isoforms in the aortic endothelium or smooth muscle did not contribute to the temporal decline in ACh-induced endothelium-dependent relaxation in sedentary OLETF rats. A significant increase in the 40-wk-old sedentary LETO and physically active OLETF rat aortic phosphorylated endothelial nitric oxide (p-eNOS)-to-eNOS ratio was observed versus 13- and 20-wk-old rats in each group that was not seen in the 40- versus 13- and 20-wk-old sedentary OLETF rats. These results suggest that temporal changes in the antioxidant system, EDHF, and cycloxygenase metabolite production in sedentary OLETF rat aortas do not contribute to the temporal decline in sedentary OLETF rat aortic ACh-induced endothelium-dependent relaxation seen with type 2 diabetes mellitus progression. We also report that physical activity in conjunction with aging in the OLETF rat results in a temporal increase in the aortic endothelial p-eNOS-to-eNOS ratio that was not seen in sedentary OLETF rats. These results suggest that the sustained aortic ACh-induced endothelium-dependent relaxation in aged physically active OLETF rats may be the result of an increase in active aortic eNOS.
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Bunker et al. (2010) studied Type 2 diabetes mellitus. Physical activity vs. Sedentary OLETF rats and sedentary LETO rats was evaluated on ACh-induced endothelium-dependent relaxation. Physical activity maintained ACh-induced endothelium-dependent relaxation in OLETF rats from 13 to 40 weeks of age, potentially due to an increase in active aortic eNOS.
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