Pressurized arteries develop active resting tone that is endothelium independent and appears to result from activation of stretch-activated Ca++ channels and voltage-gated Ca++ channels. In cerebral and coronary arteries, activation of Ca++-activated K+ channels (KCa) and voltage-dependent K+ channels (KV) acts as a negative feedback mechanism to limit Ca++-induced depolarization and contraction. The role of K+ channels in regulating resting tone in skeletal muscle resistance arteries is not known. Therefore, we tested the hypothesis that KCa, KV, inward rectifier K+ channels (KIR), and the Na+-K+ pump contribute to regulation of resting tone in soleus feed arteries (SFAs). SFAs from male Sprague-Dawley rats were isolated and cannulated with two glass micropipettes for in vitro videomicroscopic observation, and pressurized at 90 cmH2O. After development of resting tone (35.7 ± 0.5%), various blockers of K+ channels were applied in randomized order to determine the effect of specific K+ channels on resting tone. Inhibition of KCa with either tetraethylammonium (1 mM) or iberiotoxin (10 nM) did not significantly alter resting tone. Inhibition of KV with 4-aminopyridine (1 mM) also did not alter resting tone, although there was a tendency for tone to be enhanced by Kv inhibition (diameter 129.7 ± 2.6 vs 106.1 ± 2.1 μm; p = .07). Inhibition of KIR with barium chloride (30 μM) did not alter resting tone nor did inhibition of the Na+-K+ pump with ouabain (100 μM). However, combined inhibition of KIR and the Na+-K+ pump significantly increased resting tone (diameter 164.7 ± 9.7 vs 108.3 ± 10.2 μm). These data indicate that but KV, KIR, and the Na+-K+ pump each contribute to regulation of resting tone in SFAs. Unlike cerebral and coronary arteries, KCa channels do not significantly regulate tone in SFAs. These data suggest that these K+ channels are important contributors to the regulation of blood flow in skeletal muscle.
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