Effect of oxygen tension on regulation of arteriolar diameter in skeletal muscle in situ.

Abstract:

:Skeletal muscle arterioles are known to constrict upon elevation of ambient 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 arterioles 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 of indomethacin (30 microM) 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 NG-nitro-L-arginine (L-NNA, 35 mg/kg i.v.) caused arteriolar constriction by 31% (+/- 8%, n = 8). During application of L-NNA, the constrictor response to PO2 elevation was reduced to 3 +/- 2%. Administration of superoxide dismutase (SOD, 80,000 U/kg i.v.) 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 vasoconstriction in response to high ambient PO2 is not due to EDRF breakdown during its diffusion from endothelial to smooth muscle cells.

journal_name

Microvasc Res

journal_title

Microvascular research

authors

Pries AR,Heide J,Ley K,Klotz KF,Gaehtgens P

doi

10.1006/mvre.1995.1025

subject

Has Abstract

pub_date

1995-05-01 00:00:00

pages

289-99

issue

3

eissn

0026-2862

issn

1095-9319

pii

S0026-2862(85)71025-4

journal_volume

49

pub_type

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