Exercise enhances vasorelaxation in experimental obesity associated hypertension

Arvola, Pertti; Wu, Xiumin; Kähönen, Mika; Mäkynen, Heikki; Riutta, Asko; Muchá, I.; Solakivi, Tiina; Kainulainen, Heikki; Pörsti, Ilkka

doi:10.1016/s0008-6363(99)00141-8

Cited by 58 publications

(45 citation statements)

References 32 publications

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“…However, we did not find a difference in eNOS-dependent reactivity of cerebral arterioles between sedentary and exercised nondiabetic rats. This finding was surprising given the fact that others have shown that ExT increases the reactivity of peripheral blood vessels (5,11,22,37). However, in a previous study (43), we found that ExT did not influence eNOS-dependent responses of the basilar artery.…”

Section: Discussioncontrasting

confidence: 93%

“…Studies have shown that ExT can improve/ restore responses of peripheral blood vessels during chronic hypertension (5,11,26,33), types 1 and 2 diabetes (23,46,69), and heart failure (30,36). In addition, we have reported that impaired eNOS-dependent responses of the basilar artery observed in rats with type 1 diabetes (T1D) could be restored to that observed in nondiabetic rats by ExT (43).…”

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confidence: 88%

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Exercise training normalizes impaired NOS-dependent responses of cerebral arterioles in type 1 diabetic rats

Mayhan

Arrick

Patel

et al. 2011

American Journal of Physiology-Heart and Circulatory Physiology

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Mayhan WG, Arrick DM, Patel KP, Sun H. Exercise training normalizes impaired NOS-dependent responses of cerebral arterioles in type 1 diabetic rats. Am J Physiol Heart Circ Physiol 300: H1013-H1020, 2011. First published December 17, 2010; doi:10.1152/ajpheart.00873.2010.-Our goal was to examine whether exercise training (ExT) could normalize impaired nitric oxide synthase (NOS)-dependent dilation of cerebral (pial) arterioles during type 1 diabetes (T1D). We measured the in vivo diameter of pial arterioles in sedentary and exercised nondiabetic and diabetic rats in response to an endothelial NOS (eNOS)-dependent (ADP), an neuronal NOS (nNOS)-dependent [N-methyl-D-aspartate (NMDA)], and a NOS-independent (nitroglycerin) agonist. In addition, we measured superoxide anion levels in brain tissue under basal conditions in sedentary and exercised nondiabetic and diabetic rats. Furthermore, we used Western blot analysis to determine eNOS and nNOS protein levels in cerebral vessels/brain tissue in sedentary and exercised nondiabetic and diabetic rats. We found that ADP and NMDA produced a dilation of pial arterioles that was similar in sedentary and exercised nondiabetic rats. In contrast, ADP and NMDA produced only minimal vasodilation in sedentary diabetic rats. ExT restored impaired ADP-and NMDA-induced vasodilation observed in diabetic rats to that observed in nondiabetics. Nitroglycerin produced a dilation of pial arterioles that was similar in sedentary and exercised nondiabetic and diabetic rats. Superoxide levels in cortex tissue were similar in sedentary and exercised nondiabetic rats, were increased in sedentary diabetic rats, and were normalized by ExT in diabetic rats. Finally, we found that eNOS protein was increased in diabetic rats and further increased by ExT and that nNOS protein was not influenced by T1D but was increased by ExT. We conclude that ExT can alleviate impaired eNOS-and nNOS-dependent responses of pial arterioles during T1D. adenosine 5=-diphosphate; N-methyl-D-aspartate; nitroglycerin; pial arterioles; Western blot; superoxide; endothelial nitric oxide synthase; neuronal nitric oxide synthase EXERCISE TRAINING (ExT) has been shown to play a significant role in the prevention of cardiovascular-related diseases. Although the precise cellular/molecular mechanisms accounting for the favorable effects of ExT on the cardiovascular system remain uncertain, many investigators have suggested that ExT may dramatically influence vascular endothelial function. Support for this concept can be found in studies that have examined the effects of ExT on endothelial nitric oxide synthase (eNOS)-dependent vasoreactivity in animals and human subjects (22,23,27,28,60,69). These studies have reported that ExT can enhance eNOS-dependent responses of large and small blood vessels in skeletal muscle, heart, and skin. Mechanisms by which ExT potentiates nitric oxide synthase (NOS)-dependent relaxation/dilation of blood vessels are not entirely clear but are likely to be related to an increase in shear forces actin...

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Section: Discussioncontrasting

confidence: 93%

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confidence: 88%

Exercise training normalizes impaired NOS-dependent responses of cerebral arterioles in type 1 diabetic rats

Mayhan

Arrick

Patel

et al. 2011

American Journal of Physiology-Heart and Circulatory Physiology

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“…However, a meta-analysis study of exercise in type II diabetic patients showed that exercise failed to decrease blood pressure in this patient subset (64). A longer duration of exercise (14-22 wk) has been shown to reduce systolic blood pressure in these rats using the tail cuff method (4,54). It is possible that the shorter duration of exercise (8 wk) in our study precluded us from observing a decrease in blood pressure.…”

Section: Discussionmentioning

confidence: 99%

Exercise reduces oxidative stress but does not alleviate hyperinsulinemia or renal dopamine D₁receptor dysfunction in obese rats

Muhammad

Lokhandwala

Banday

2011

American Journal of Physiology-Renal Physiology

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“…These observations are confirmed in animal studies. In obese Zucker (fa/fa) rats characterized by moderate hypertension (3,4), hyperlipidemia (5,6), and insulin resistance/impaired glucose tolerance (7,8), exercise improves insulin sensitivity (9) and reduces blood lipids (10), blood pressure (4), and obesity (11,12).…”

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confidence: 99%

Long-Term AICAR Administration Reduces Metabolic Disturbances and Lowers Blood Pressure in Rats Displaying Features of the Insulin Resistance Syndrome

et al. 2002

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The insulin resistance syndrome is characterized by several risk factors for cardiovascular disease. Chronic chemical activation of AMP-activated protein kinase by the adenosine analog 5-aminoimidazole-4-carboxamide-1-␤-D-ribofuranoside (AICAR) has been shown to augment insulin action, upregulate mitochondrial enzymes in skeletal muscles, and decrease the content of intraabdominal fat. Furthermore, acute AICAR exposure has been found to reduce sterol and fatty acid synthesis in rat hepatocytes incubated in vitro as well as suppress endogenous glucose production in rats under euglycemic clamp conditions. To investigate whether chronic AICAR administration, in addition to the beneficial effects on insulin sensitivity, is capable of improving other phenotypes associated with the insulin resistance syndrome, obese Zucker (fa/fa) rats (n ‫؍‬ 6) exhibiting insulin resistance, hyperlipidemia, and hypertension were subcutaneously injected with AICAR (0.5 mg/g body wt) daily for 7 weeks. Obese control rats were either pair-fed (PF) (n ‫؍‬ 6) or ad libitum-fed (AL) (n ‫؍‬ 6). Lean Zucker rats (fa/؊) (n ‫؍‬ 8) served as a reference group. AICAR administration significantly reduced plasma triglyceride levels (P < 0.01 for AICAR vs. AL, and P ‫؍‬ 0.05 for AICAR vs. PF) and free fatty acids (P < 0.01 for AICAR vs. AL, and P < 0.05 for AICAR vs. PF) and increased HDL cholesterol levels (P < 0.01 for AICAR vs. AL and PF). AICAR treatment also lowered systolic blood pressure by 14.6 ؎ 4.3 mmHg (P < 0.05), and AICAR-treated animals exhibited a tendency toward decreased intra-abdominal fat content. Furthermore, AICAR administration normalized the oral glucose tolerance test and decreased fasting concentrations of glucose and insulin close to the level of the lean animals. Finally, in line with previous findings, AICAR treatment was also found to enhance GLUT4 protein expression and to increase maximally insulin-stimulated glucose transport in primarily white fast-twitch muscles. Our data provide strong evidence that longterm administration of AICAR improves glucose tolerance, improves the lipid profile, and reduces systolic blood pressure in an insulin-resistant animal model. The present study gives additional support to the hypothesis that AMPK activation might be a potential future pharmacological strategy for treating the insulin resistance syndrome.

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Exercise enhances vasorelaxation in experimental obesity associated hypertension

Cited by 58 publications

References 32 publications

Exercise training normalizes impaired NOS-dependent responses of cerebral arterioles in type 1 diabetic rats

Exercise training normalizes impaired NOS-dependent responses of cerebral arterioles in type 1 diabetic rats

Exercise reduces oxidative stress but does not alleviate hyperinsulinemia or renal dopamine D₁receptor dysfunction in obese rats

Long-Term AICAR Administration Reduces Metabolic Disturbances and Lowers Blood Pressure in Rats Displaying Features of the Insulin Resistance Syndrome

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Exercise enhances vasorelaxation in experimental obesity associated hypertension

Cited by 58 publications

References 32 publications

Exercise training normalizes impaired NOS-dependent responses of cerebral arterioles in type 1 diabetic rats

Exercise training normalizes impaired NOS-dependent responses of cerebral arterioles in type 1 diabetic rats

Exercise reduces oxidative stress but does not alleviate hyperinsulinemia or renal dopamine D1receptor dysfunction in obese rats

Long-Term AICAR Administration Reduces Metabolic Disturbances and Lowers Blood Pressure in Rats Displaying Features of the Insulin Resistance Syndrome

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Exercise reduces oxidative stress but does not alleviate hyperinsulinemia or renal dopamine D₁receptor dysfunction in obese rats