Carbon monoxide does not contribute to vascular tonus improvement in exercise-trained rats with chronic nitric oxide synthase inhibition.
Nitric Oxide(2017)
Abstract
Carbon monoxide (CO), an end product of heme oxygenase (HO) that is involved in the regulation of vascular tonus, may show a compensatory effect in nitric oxide (NO) deficiency. This study aimed to assess the effect of the HO/CO system on the vascular tone in exercise-trained rats with hypertension induced by chronic NO synthase (NOS) inhibition. Hypertension was induced by N-nitro-l-arginine methyl ester (25 mg/kg/day in drinking water), and exercise training comprised swimming 1 h/day, 5 days/week, for 6 weeks. Systolic blood pressure (BP) was measured weekly using a tail-cuff method. The effects of hypertension and/or exercise-training on the constriction and relaxation responses of the thoracic aorta and resistance arteries of the mesenteric and gastrocnemius vascular beds were evaluated. NOS inhibition produced a gradually developed hypertension, and the magnitude of the increase in BP was significantly attenuated by exercise training. Although phenylephrine (Phe)-induced contraction responses of aorta incubated with an HO-1 inhibitor were reduced in hypertensive animals, there was no difference in the hypertensive-exercise group. However, thoracic aortas in the hypertensive-exercise group exhibited significantly more relaxation in response to a CO donor. There was no change in Phe-induced contraction with or without HO inhibition CO donor relaxation responses in both resistance arteries. These results suggest that the HO/CO system does not contribute to diminishing BP by exercise training in a NOS inhibition-induced hypertension model.
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Key words
Carbon monoxide,Hypertension,Exercise,Heme oxygenase,Nitric oxide synthase
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