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Potassium channel regulation of vasomotor responses in rat soleus feed arteries after short‐term exercise training
Author(s) -
Atkins Scott Aaron,
Onishi Kentaro,
Jasperse Jeffrey L.
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.4.a813-a
Subject(s) - sed , chemistry , vasomotor , ouabain , medicine , endocrinology , potassium , constriction , sodium , organic chemistry
We previously reported that short term exercise training (STEx) alters the vasomotor responses of rat soleus feed arteries (SFA) to 20 mM KCl as SFA from sedentary (SED) constricted while SFA from STEx dilated (FASEB J 19:A1220, 2005). The purpose of this study was to determine if the activity of specific K+ channels is modified by STEx. Male Sprague‐Dawley rats were cage confined or ran on a motorized treadmill four weeks (30 m/min, 10% grade, 60 min/d, 5 d/wk). SFA were isolated and cannulated with two glass micropipettes for in vitro videomicroscopic observation, and pressurized at 90 cmH2O. Dilation to 10 mM KCl tended to be increased by STEx (SED 13.9 ± 2.3% and STEx 26.6 ± 1.3%; p=0.07). Inhibition of inward rectifier K+ channels (KIR) with BaCl2 (30 uM) did not alter the response in SED but reduced dilation in STEx (4.8 ± 3.3%). The Na+/K+ ATPase inhibitor ouabain (100 uM) did not alter dilation to 10 mM KCl in SED or STEx. Combined blockade with BaCl2 and ouabain did not alter the dilation in SED but abolished the dilation in STEx (−0.5 ± 3.6%). With 20 mM KCl, SED constricted 5.9 ± 1.8% while STEx dilated 3.9 ± 1.2% (p=0.12). In SED, ouabain had no effect but BaCl2 (18.7 ± 1.8%; p=0.08) and BaCl2 + ouabain (24.9 ± 1.5%) increased constriction. In STEx, application of all inhibitors changed dilation to constriction (BaCl2 17.5 ± 3.4%, ouabain 10.1 ± 1.9%, BaCl2 + ouabain 17.7 ± 2.1%). These data indicate that STEx increases activity of KIR at 10 mM KCl and of Na+/K+ ATPase at 20 mM KCl. This suggests that KIR modifications in response to STEx may be responsible for the difference between STEx and SED SFA responses to physiologically relevant K+ concentrations (10 mM).