Intense exercise training is not effective to restore the endothelial NO-dependent relaxation in STZ-diabetic rat aorta

Zouhair Tabka,Solène Le Douairon Lahaye,Bernard Saïag,Sophie Vincent,Mohamed Sami Zguira,Ludivine Malarde

doi:10.1186/1475-2840-12-32

Zouhair Tabka, Solène Le Douairon Lahaye + Show 4 more

Open Access

https://doi.org/10.1186/1475-2840-12-32

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Abstract

BackgroundThe aim of this study was to examine the effects of intense physical training on vascular function in streptozotocin-diabetic rats. We focused on the endothelium-dependent relaxation (EDR) induced by acetylcholine (ACh) and stable ADP adenosine-5′- O – (2-thiodiphosphate) (ADPβS).MethodsControl or diabetic male Wistar rats (n=44) were randomly assigned to sedentary or trained groups. The training program consisted in a regular period of running on a treadmill during 8 weeks (10° incline and up to 25 m/min, 60 min/day). The reactivity of isolated thoracic aorta rings of healthy, diabetic and/or trained has been tested.ResultsACh and ADPβS-induced EDR were observed in phenylephrine (PE) pre-contracted vessels. As compared to sedentary control group, diabetic rats showed an increase in PE-induced contraction and a decrease in ACh and ADPβS-induced EDR (p<0.05). Moreover, there were no increase in ACh and ADPβS-induced EDR in diabetic rats. N-Nitro-L-Arginine Methyl Ester inhibited the nitric oxide synthase in diabetic and control rats, thereby resulting in a strong inhibition of the EDR induced by ACh and ADPβS (10-6 M).ConclusionDiabetes induced an endothelium dysfunction. Nevertheless, our intense physical training was not effective to restore the aorta endothelial function.

Highlights

The endothelium provides a cellular lining to all blood vessels in the circulatory system and forms a structural barrier between the vascular space and the tissues
This study aimed to evaluate the effects of intense exercise training on endothelium-dependent relaxation (EDR) in diabetic rats as well as the NO-EDR induced by ACh and ADPβS
ACh and ADPβS-induced EDRs are mediated via NO pathway in control and STZ-diabetic rats Our results demonstrated that the NO°/EDRF pathway is involved in the molecular mechanism of these EDR as described in other studies [29,31]

Summary

Introduction

The endothelium provides a cellular lining to all blood vessels in the circulatory system and forms a structural barrier between the vascular space and the tissues. Endothelial cells (ECs) regulate vascular flow and basal vasomotor tone by the highly controlled release of vasodilators (nitric oxide (NO) and prostacyclin (PGI2)) and vasoconstrictors [1]. NO is generated in ECs by the oxidation of L-arginine to L-citrulline by the NO synthases (NOS) enzymes family. The endothelial NOS (eNOS) isoform is constitutively active but is further induced by receptor dependent agonist such as thrombin, adenosine 5-diphosphate, bradykinin and substance P [2,3]. It has been established that diabetes is associated with vascular dysfunctions caused by an impairment of EDR [13,14]. The aim of this study was to examine the effects of intense physical training on vascular function in streptozotocin-diabetic rats. We focused on the endothelium-dependent relaxation (EDR) induced by acetylcholine (ACh) and stable ADP adenosine-50- O – (2-thiodiphosphate) (ADPβS)

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