Short-term exercise training increases ACh-induced relaxation and eNOS protein in porcine pulmonary arteries

Citation
Lr. Johnson et al., Short-term exercise training increases ACh-induced relaxation and eNOS protein in porcine pulmonary arteries, J APP PHYSL, 90(3), 2001, pp. 1102-1110
Citations number
22
Categorie Soggetti
Physiology
Journal title
JOURNAL OF APPLIED PHYSIOLOGY
ISSN journal
87507587 → ACNP
Volume
90
Issue
3
Year of publication
2001
Pages
1102 - 1110
Database
ISI
SICI code
8750-7587(200103)90:3<1102:SETIAR>2.0.ZU;2-L
Abstract
Short-term exercise training increases ACh-induced relaxation and eNOS prot ein in porcine pulmonary arteries. J Appl Physiol 90: 1102-1110, 2001.-We t ested the hypothesis that short-term; exercise (STEx) training and the asso ciated increase in pulmonary blood flow during bouts of exercise cause enha nced endothelium-dependent vasorelaxation in porcine pulmonary arteries and increased expression of endothelial cell nitric oxide synthase (eNOS) and superoxide dismutase-1 (SOD-1) protein. Mature, female Yucatan miniature sw ine exercised 1 h twice daily on a motorized treadmill for 1 wk (STEx group , n = 7); control pigs (Sed, n = 6) were kept in pens. Pulmonary arteries w ere isolated from the left caudal lung lobe, and vasomotor responses were d etermined in vitro. Arterial tissue from the distal portion of this pulmona ry artery was processed for immunoblot analysis. Maximal endothelium-depend ent (ACh-stimulated) relaxation was greater in STEx (71 +/- 5%) than in Sed (44 +/- 6%) arteries (P < 0.05), and endothelium-independent (sodium nitro prusside-mediated) responses did not differ. Sensitivity to ACh was not alt ered by STEx training. Immunoblot analysis indicated a 3.9-fold increase in eNOS protein in pulmonary artery tissue from STEx pigs (P < 0.05) with no change in SOD-1 or glyceraldehyde-3-phosphate dehydrogenase protein levels. We conclude that STEx training enhances ACh-stimulated vasorelaxation in p ulmonary arterial tissue and that this adaptation is associated with increa sed expression of eNOS protein.