Ar. Pries et al., EFFECT OF OXYGEN-TENSION ON REGULATION OF ARTERIOLAR DIAMETER IN SKELETAL-MUSCLE IN-SITU, Microvascular research, 49(3), 1995, pp. 289-299
Skeletal muscle arterioles are known to constrict upon elevation of am
bient PO2. While several studies have shown that the endothelium plays
an important role in this response, it is not clear how this response
is mediated. We examined the oxygen-induced constriction of arteriole
s in the rat spinotrapezius muscle. Elevation of superfusion solution
PO2 from about 15 to 150 mm Hg caused arteriolar constriction by 25% (
+/-3%, n = 18). Inhibition of prostaglandin synthesis by superfusion o
f indomethacin (30 mu M) produced vasoconstriction by 28% (+/-9.5%, n
= 5), but left the PO2 response unaffected. Blockade of the synthesis
of endothelium-derived relaxing factor (EDRF) by N-G-nitro-L-arginine
(L-NNA, 35 mg/kg iv) caused arteriolar constriction by 31% (+/-8%, n =
8). During application of L-NNA, the constrictor response to PO2 elev
ation was reduced to 3 +/- 2%. Administration of superoxide dismutase
(SOD, 80,000 U/kg iv) did not affect the PO2 response. It is concluded
that in small arterioles of skeletal muscle both EDRF and prostanoids
sustain a significant basal dilatation. The dilatory effects of EDRF
but not of prostaglandins are strongly dependent on PO2. The vasoconst
riction in response to high ambient PO2 is not due to EDRF breakdown d
uring its diffusion from endothelial to smooth muscle cells. (C) 1995
Academic Press, Inc.