EXERCISE TRAINING INCREASES K-CHANNEL CONTRIBUTION TO REGULATION OF CORONARY ARTERIAL TONE()

Citation
Dk. Bowles et al., EXERCISE TRAINING INCREASES K-CHANNEL CONTRIBUTION TO REGULATION OF CORONARY ARTERIAL TONE(), Journal of applied physiology, 84(4), 1998, pp. 1225-1233
Citations number
42
Categorie Soggetti
Physiology,"Sport Sciences
ISSN journal
87507587
Volume
84
Issue
4
Year of publication
1998
Pages
1225 - 1233
Database
ISI
SICI code
8750-7587(1998)84:4<1225:ETIKCT>2.0.ZU;2-0
Abstract
The present study examined whether regulation of coronary tone in cond uit arteries (>1.0 mm ID) is altered by exercise training. Yucatan min iature swine were treadmill trained for 16-20 wk (Ex) and compared wit h sedentary counterparts (Sed). Endothelium-denuded arterial rings wer e stretched to optimal length and allowed to equilibrate for BO min. I nhibition 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 twofo ld in Ex compared with Sed group. Perforated patch-clamp experiments o n isolated smooth muscle cells demonstrated no effect of exercise trai ning 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 i n Sed by addition of the Ca2+-channel agonist BAY K 8644. In conclusio n, the greater response to K+-channel blockers after exercise training is consistent with an increased contribution of Kf channels to regula tion of basal tone in conduit coronary arteries. The lack of an effect of training on K+ current characteristics or membrane potential respo nses in isolated cells suggests that a requisite factor for enhanced K +-channel activation in arteries from Ex, possibly stretch, is absent in isolated cells.