Potassium Channel Role in EDHF‐Induced Dilation of Soleus Feed Arteries from Sedentary and Short‐term Exercise Trained Rats

Endothelium‐derived hyperpolarizing factors (EDHF) may act through one or more K + channels. We tested the hypothesis that specific K + channels (K V , K ATP , K IR and Na‐K pump) mediate the EDHF response and that short term exercise training (STEX)(4 wks) increases the K + channel role. STEX rats ran on a treadmill at 30m/min for 1 hr/d, 5 d/wk. Soleus feed arteries (n=37) were isolated, cannulated and pressurized at 90 cm H 2 0. STEX did not alter the effect of K + channel inhibition on ACh (10 −9 ‐10 −4 M) dilation, so data from SED and STEX rats are combined. In Group 1, ACh caused 87.3 ± 2.8% dilation, which was reduced by K V (1mM 4‐aminopyradine) inhibition to 80.1 ± 3.5% dilation, and reduced further by combined K v and K ATP inhibition (50 μM glibenclamide) (41.5 ± 7.5%). In Group 2, ACh caused 80.6 ± 7.2% dilation. NO (300 μM L‐NNA )and PGI 2 (5 μM indomethacin) inhibition reduced dilation to 31.4 ±9.5%. Adding K V inhibition did not further decrease dilation, but adding combined K V and K ATP inhibition reduced dilation to 8.3 ± 3.7%. In Group 3, ACh caused 82.6 ± 3.5% dilation, which was not reduced by Na‐K pump (100 μM ouabain) inhibition. Na‐K pump and K IR (30 μM BaCl 2 ) inhibition reduced dilation to 64.6 ± 5.9%. NO and PGI 2 inhibition reduced dilation to 32.7 ± 7.9%. Combined Na‐K pump, K IR , NO and PGI 2 inhibition reduced dilation to 16.4 ± 3.9%. Collectively, these data indicate that K V , K ATP , K IR and the Na‐K pump all contribute to EDHF dilation.