Effect of exercise training on resistance arteries in rats with chronic NOS inhibition.
Regular exercise has blood pressure-lowering effects, as shown in different types of experimental hypertension models in rats, including the nitric oxide synthase (NOS) inhibition model. We aimed to investigate possible mechanisms implicated in the exercise effect by evaluating the vasoreactivity of resistance arteries. Exercise effects on agonist-induced vasodilatory responses and flow-mediated dilation were evaluated in vessel segments of the rat chronic NOS inhibition model. Normotensive and hypertensive rats were subjected to swimming exercise (1 h/day, 5 days/wk, 6 wk), while rats in other sedentary and hypertensive groups did not. Hypertension was induced by oral administration of the nonselective NOS inhibitor l-NAME (25 mg/kg day) for 6 wk. Systolic blood pressure, as measured by the tail-cuff method, was significantly decreased by the training protocol in exercising hypertensive rats. The vasoreactivity of resistance arteries was evaluated by both wire and pressure myography studies. An impaired nitric oxide-mediated relaxation pathway in untrained hypertensive rats led to decreased relaxation responses in vessels with intact endothelium. Exercise training significantly improved the responses to acetylcholine and flow-mediated dilation in exercise-trained hypertensive rats in parallel with a decrease in blood pressure. On the other hand contraction (norepinephrine and KCl) and relaxation (sodium nitroprusside) responses of vascular smooth muscle were not different between the groups. Vascular endothelial NOS protein expression was found to be increased in both exercising groups. In conclusion, these results revealed evidence of an increased role of the nitric oxide-dependent relaxation pathway in exercising hypertensive rats.
Kuru
Oktay
O
School of Health Sciences, Mugla University, Mugla, Turkey.
Sentürk
Umit Kemal
UK
Koçer
Günnur
G
Ozdem
Sadi
S
Başkurt
Oğuz K
OK
Cetin
Arzu
A
Yeşilkaya
Akin
A
Gündüz
Filiz
F
D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D001158:Arteries / Q000187:drug effects* / Q000502:physiology*; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D001835:Body Weight / Q000502:physiology; D004305:Dose-Response Relationship, Drug; D004791:Enzyme Inhibitors / Q000494:pharmacology*; D005260:Female; D005987:Glyceraldehyde-3-Phosphate Dehydrogenases / Q000378:metabolism; D007527:Isoenzymes / Q000037:antagonists & inhibitors / Q000378:metabolism; D009126:Muscle Relaxation / Q000187:drug effects / Q000502:physiology; D009213:Myography; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors*; D009599:Nitroprusside / Q000494:pharmacology; D009638:Norepinephrine / Q000494:pharmacology; D010805:Physical Conditioning, Animal / Q000502:physiology*; D051381:Rats; D017208:Rats, Wistar; D014655:Vascular Resistance / Q000187:drug effects* / Q000502:physiology*; D014662:Vasoconstrictor Agents / Q000494:pharmacology; D014664:Vasodilation / Q000187:drug effects / Q000502:physiology; D014665:Vasodilator Agents / Q000494:pharmacology
D004791:Enzyme Inhibitors; D007527:Isoenzymes; D014662:Vasoconstrictor Agents; D014665:Vasodilator Agents; D009599:Nitroprusside; D019001:Nitric Oxide Synthase; D005987:Glyceraldehyde-3-Phosphate Dehydrogenases; D000109:Acetylcholine; D019331:NG-Nitroarginine Methyl Ester; D009638:Norepinephrine