Literature DB >> 18945274

Involvement of endothelin-1 in habitual exercise-induced increase in arterial compliance.

S Maeda1, J Sugawara, M Yoshizawa, T Otsuki, N Shimojo, S Jesmin, R Ajisaka, T Miyauchi, H Tanaka.   

Abstract

AIM: Habitual aerobic exercise results in a significant increase in central arterial compliance. Endothelin-1 (ET-1) is a potent endothelium-derived vasoconstrictor peptide and could play a role in mediating the habitual aerobic exercise-induced increase in central arterial compliance. The aim of the present study was to examine whether ET-1 is involved in the mechanisms underlying the increase in central arterial compliance with aerobic exercise training.
METHODS: Seven apparently healthy middle-aged and older (60 +/- 3 years) adults underwent systemic endothelin-A/B (ET(A/B))-receptor blockade (500 mg of Tracleer) before and after 12 weeks of aerobic exercise training (70 +/- 1% of maximal heart rate, 44 +/- 2 min day(-1), 4.4 +/- 0.1 days week(-1)).
RESULTS: Basal carotid arterial compliance (via simultaneous B-mode ultrasound and arterial applanation tonometry on the common carotid artery) increased significantly after exercise training. Resting plasma ET-1 concentration decreased significantly after exercise training. Before exercise intervention, carotid arterial compliance increased significantly with the administration of the ET(A/B)-receptor blockade. After training, however, increases in carotid arterial compliance previously observed with the ET(A/B)-receptor blockade before training were abolished.
CONCLUSIONS: Regular aerobic exercise training enhances central arterial compliance in middle-aged and older humans. The increase in arterial compliance was associated with the corresponding reduction in plasma ET-1 concentration as well as the elimination of ET-1-mediated vascular tone. These results suggest that reductions in ET-1 may be an important mechanism underlying the beneficial effect of exercise training on central artery compliance.

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Year:  2008        PMID: 18945274      PMCID: PMC2693217          DOI: 10.1111/j.1748-1716.2008.01909.x

Source DB:  PubMed          Journal:  Acta Physiol (Oxf)        ISSN: 1748-1708            Impact factor:   6.311


  27 in total

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