© 1999 by European Society of Cardiology
Copyright © 1999, European Society of Cardiology
Exercise enhances vasorelaxation in experimental obesity associated hypertension
aDepartments of Pharmacological Sciences, University of Tampere, Medical School, Tampere, Finland
bMedical Biochemistry, University of Tampere, Medical School, Tampere, Finland
cInstitute of Medical Technology, University of Tampere, Medical School, Tampere, Finland
dDepartments of Internal Medicine, Tampere University Hospital, Tampere, Finland
eClinical Physiology, Tampere University Hospital, Tampere, Finland
fClinical Chemistry, Tampere University Hospital, Tampere, Finland
gDepartment of Internal Medicine, University Hospital, Helsinki, Finland
hInstitute of Isotopes Co., Budapest, Hungary
* Corresponding author. Tel.: +358-3-215-6111; fax: +358-3-215-6170 blilpo{at}uta.fi
Objective: Regular exercise is recommended for the non-pharmacological treatment of hypertension, but the mechanisms underlying the lowering of blood pressure remain controversial. Therefore, we studied the effects of 22-week-long training on blood pressure, arterial reactivity, and metabolic abnormalities in a model of genetic obesity and moderate hypertension. Methods: Obese and lean Zucker rats were subjected to treadmill exercise from 8 to 30 weeks of age. Blood pressures were measured by the tail-cuff method, and urine was collected in metabolic cages. At the end of the study, the samples for biochemical determinations were taken, and reactivity of isolated mesenteric and carotid arterial rings was examined in standard organ chambers. Results: The exercise prevented the elevation of blood pressure which was observed in non-exercised obese Zucker rats, and also reduced blood pressure in the lean rats. The relaxations of norepinephrine-preconstricted mesenteric and carotid arterial rings to acetylcholine and nitroprusside were clearly improved by exercise in the obese rats. In the lean rats exercise enhanced vasorelaxation to nitroprusside in the mesenteric and carotid rings, and to acetylcholine in the carotid preparations. The exercise-induced improvement of endothelium-mediated dilatation to acetylcholine was abolished by nitric oxide synthesis inhibition with NG-nitro-L-arginine methyl ester, but not by cyclooxygenase inhibition with diclofenac or functional inhibition of endothelium-dependent hyperpolarization by precontractions with KCl. The urinary excretion of the systemic prostacyclin metabolite (2,3-dinor-6-ketoprostaglandin F1
) was increased two-fold by exercise in the obese and lean rats, whereas that of the thromboxane A2 metabolite (11-dehydrothromboxane B2) remained unaffected. Treadmill training reduced blood glucose, cholesterol, and triglycerides, but did not affect the high levels of insulin in obese Zucker rats. Conclusions: These results suggest that the antihypertensive effect of long-term exercise in experimental obesity related hypertension is associated with improved vasodilatation. This is expressed as enhanced relaxation via endogenous and exogenous nitric oxide, and increased endothelial prostacyclin production. The improved control of arterial tone after training could be attributed to the alleviation of hyperlipidemia and insulin resistance, whereas hyperinsulinaemia per se remained unaffected.
KEYWORDS Endothelial factors; Exercise; Hypertension; Nitric oxide; Obesity