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Background  ATP-sensitive K +  channels (K ATP  channels), NO, prostaglandins, 20-HETE and L-type Ca 2+  channels have all been suggested to be involved in oxygen sensing in skeletal muscle arterioles, but the role of the individual mechanisms remain controversial. We aimed to establish the importance of these mechanisms for oxygen sensing in arterioles in an  in vivo  model of metabolically active skeletal muscle. For this purpose we utilized the exteriorized cremaster muscle of anesthetized mice, in which the cremaster muscle was exposed to controlled perturbation of tissue  P O 2 .    Results  Change from “high” oxygen tension ( P O 2  = 153.4 ± 3.4 mmHg) to “low” oxygen tension ( P O 2  = 13.8 ± 1.3 mmHg) dilated cremaster muscle arterioles from 11.0 ± 0.4 μm to 32.9 ± 0.9 μm (n = 28, P < 0.05). Glibenclamide (K ATP  channel blocker) caused maximal vasoconstriction, and abolished the dilation to low oxygen, whereas the K ATP  channel opener cromakalim caused maximal dilation and prevented the constriction to high oxygen. When adding cromakalim on top of glibenclamide or vice versa, the reactivity to oxygen was gradually restored. Inhibition of L-type Ca 2+  channels using 3 μM nifedipine did not fully block basal tone in the arterioles, but rendered them unresponsive to changes in  P O 2 . Inhibition of the CYP450-4A enzyme using DDMS blocked vasoconstriction to an increase in  P O 2 , but had no effect on dilation to low  P O 2 .    Conclusions  We conclude that: 1) L-type Ca 2+  channels are central to oxygen sensing, 2) K ATP  channels are permissive for the arteriolar response to oxygen, but are not directly involved in the oxygen sensing mechanism and 3) CYP450-4A mediated 20-HETE production is involved in vasoconstriction to high  P O 2 .

Significance of KATP channels, L-type Ca2+ channels and CYP450-4A enzymes in oxygen sensing in mouse cremaster muscle arterioles In vivo