title: Exercise training increases K+-channel contribution to regulation of coronary arterial tone.
abstract: The present study examined whether regulation of coronary tone in conduit arteries (>1.0 mm ID) is altered by exercise training. Yucatan miniature swine were treadmill trained for 16-20 wk (Ex) and compared with sedentary counterparts (Sed). Endothelium-denuded arterial rings were stretched to optimal length and allowed to equilibrate for 60 min. Inhibition of either Ca2+-activated channels [1 mM tetraethylammonium (TEA) or 10 nM iberiotoxin (IBTX)] or voltage-dependent K+ channels [1 mM 4-aminopyridine (4-AP)] significantly increased resting tension in both groups; however, the effect of all K+-channel blockers was greater in Ex. Addition of 1 mM sodium nitroprusside reduced resting tension in both groups, confirming the presence of active basal tone; however, sodium nitroprusside-sensitive tone was increased approximately twofold in Ex compared with Sed group. Perforated patch-clamp experiments on isolated smooth muscle cells demonstrated no effect of exercise training on whole cell TEA-sensitive, 4-AP-sensitive, or basal K+ current. Similarly, whereas TEA, 4-AP, and IBTX all decreased resting membrane potential, there was no difference in depolarization between groups. The greater effect of TEA on resting tension in Ex could be mimicked in Sed by addition of the Ca2+-channel agonist BAY K 8644. In conclusion, the greater response to K+-channel blockers after exercise training is consistent with an increased contribution of K+ channels to regulation of basal tone in conduit coronary arteries. The lack of an effect of training on K+ current characteristics or membrane potential responses in isolated cells suggests that a requisite factor for enhanced K+-channel activation in arteries from Ex, possibly stretch, is absent in isolated cells.
authors.affiliation: Vascular Biology Laboratory, Dalton Cardiovascular Research Center, and Departments of Physiology and Veterinary Biomedical Sciences, University of Missouri, Columbia, Missouri 65211, USA. dcrcdb@showme.missouri.edu
authors.forename: D K
authors.initials: DK
authors.lastname: Bowles
authors.forename: M H
authors.initials: MH
authors.lastname: Laughlin
authors.forename: M
authors.initials: M
authors.lastname: Sturek
mesh_terms: D015761:4-Aminopyridine / Q000494:pharmacology; D000818:Animals; D002118:Calcium / Q000378:metabolism; D003331:Coronary Vessels / Q000187:drug effects / Q000502:physiology*; D004558:Electric Stimulation; D005260:Female; D066298:In Vitro Techniques; D007537:Isometric Contraction / Q000187:drug effects / Q000502:physiology; D009129:Muscle Tonus / Q000187:drug effects / Q000502:physiology*; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000502:physiology*; D018408:Patch-Clamp Techniques; D010455:Peptides / Q000494:pharmacology; D010805:Physical Conditioning, Animal / Q000502:physiology*; D015221:Potassium Channels / Q000187:drug effects / Q000502:physiology*; D013552:Swine; D013757:Tetraethylammonium Compounds / Q000494:pharmacology
chemical_list: D010455:Peptides; D015221:Potassium Channels; D013757:Tetraethylammonium Compounds; C064719:iberiotoxin; D015761:4-Aminopyridine; D002118:Calcium