title: Exercise training-enhanced, endothelium-dependent dilation mediated by altered regulation of BK(Ca) channels in collateral-dependent porcine coronary arterioles.
abstract: OBJECTIVE
  Test the hypothesis that exercise training increases the contribution of BK(Ca) channels to endothelium-mediated dilation in coronary arterioles from collateral-dependent myocardial regions of chronically occluded pig hearts and may function downstream of H2O2.
  
  
  METHODS
  An ameroid constrictor was placed around the proximal left circumflex coronary artery to induce gradual occlusion in Yucatan miniature swine. Eight weeks postoperatively, pigs were randomly assigned to sedentary or exercise training (treadmill; 14 week) regimens.
  
  
  RESULTS
  Exercise training significantly enhanced bradykinin-mediated dilation in collateral-dependent arterioles (~125 μm diameter) compared with sedentary pigs. The BK(Ca) -channel blocker, iberiotoxin alone or in combination with the H2O2 scavenger, polyethylene glycol catalase, reversed exercise training-enhanced dilation in collateral-dependent arterioles. Iberiotoxin-sensitive whole-cell K+ currents (i.e., BK(Ca)-channel currents) were not different between smooth muscle cells of nonoccluded and collateral-dependent arterioles of sedentary and exercise trained groups.
  
  
  CONCLUSIONS
  These data provide evidence that BK(Ca)-channel activity contributes to exercise training-enhanced endothelium-dependent dilation in collateral-dependent coronary arterioles despite no change in smooth muscle BK(Ca)-channel current. Taken together, our findings suggest that a component of the bradykinin signaling pathway, which stimulates BK(Ca) channels, is enhanced by exercise training in collateral-dependent arterioles and suggest a potential role for H2O2 as the mediator.
authors.affiliation: Department of Veterinary Physiology & Pharmacology, Texas A&M University, College Station, Texas, USA.
authors.forename: Wei
authors.initials: W
authors.lastname: Xie
authors.forename: Janet L
authors.initials: JL
authors.lastname: Parker
authors.forename: Cristine L
authors.initials: CL
authors.lastname: Heaps
mesh_terms: D000818:Animals; D001160:Arterioles / Q000502:physiology*; D001920:Bradykinin / Q000494:pharmacology / Q000502:physiology; D002374:Catalase / Q000378:metabolism / Q000494:pharmacology; D003097:Collateral Circulation / Q000502:physiology; D003326:Coronary Circulation / Q000502:physiology*; D004730:Endothelium, Vascular / Q000502:physiology*; D005260:Female; D006861:Hydrogen Peroxide / Q000378:metabolism; D051036:Large-Conductance Calcium-Activated Potassium Channels / Q000819:agonists / Q000037:antagonists & inhibitors / Q000502:physiology*; D009131:Muscle, Smooth, Vascular / Q000502:physiology; D018408:Patch-Clamp Techniques; D010455:Peptides / Q000494:pharmacology; D010805:Physical Conditioning, Animal / Q000502:physiology*; D011092:Polyethylene Glycols / Q000494:pharmacology; D011188:Potassium / Q000378:metabolism; D011897:Random Allocation; D013482:Superoxide Dismutase / Q000378:metabolism; D013552:Swine; D013556:Swine, Miniature; D014664:Vasodilation / Q000502:physiology*
chemical_list: D051036:Large-Conductance Calcium-Activated Potassium Channels; D010455:Peptides; C070295:catalase-polyethylene glycol; D011092:Polyethylene Glycols; C064719:iberiotoxin; D006861:Hydrogen Peroxide; D002374:Catalase; D013482:Superoxide Dismutase; D011188:Potassium; D001920:Bradykinin