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. 1995 Nov 15;489(Pt 1):225–234. doi: 10.1113/jphysiol.1995.sp021044

The role of adenosine in mediating vasodilatation in mesenteric circulation of the rat in acute and chronic hypoxia.

R Mian 1, J M Marshall 1
PMCID: PMC1156806  PMID: 8583406

Abstract

1. We have compared the roles of adenosine in mediating dilator responses to acute hypoxia in mesenteric microcirculation of control, normoxic (N) rats and in chronically hypoxic (CH) rats kept in an hypoxic chamber at 10% O2 for 3-4 weeks. 2. In fifteen N rats, acute hypoxia (breathing 6% O2 for 3 min) induced mean increases in the diameter of arterial vessels of mesentery (whose internal diameter was 10-350 microns) of 8.0 +/- 1.9% (mean +/- S.E.M.) and of venous vessels (whose internal diameter was 12-360 microns) of 10.4 +/- 2.6%. These diameter changes were reduced by approximately 30% when the adenosine receptor antagonist 8-sulpho-phenyltheophylline (8-SPT, 10(-3) M) was applied topically to the mesentery. 3. In a further six N rats, topical application of graded concentrations of adenosine (10(-7)-10(-3) M) to the mesentery evoked graded increases in the diameter of all arterial and venous vessels, maximum increases with 10(-3) M being 12.5 +/- 3.3 and 8.4 +/- 4.3%, respectively; these responses were abolished by 8-SPT. 4. By contrast, in fourteen CH rats, the smaller change in inspirate from 10 to 8% O2 induced increases in diameter of arterial and venous vessels which had control diameters that were comparable to those of N rats, of 14.1 +/- 2.4 and 12.9 +/- 2.7%, respectively, and which were virtually equivalent to the responses induced by topical application of 10(-3) M adenosine (13.3 +/- 1.3 and 16.3 +/- 2.0% in arterial and venous vessels, respectively). The changes induced by acute hypoxia were abolished by 8-SPT, as were those induced by adenosine. 5. These results suggest that in the intestinal mesentery, where the blood vessels have negligible tissue parenchyma around them, locally released or synthesized adenosine makes a substantial contribution to the dilatation that is evoked in arteriolar vessels by acute hypoxia and to the active dilatation, or passive distension of the venous vessels. The results also suggest that this contribution is accentuated in chronic hypoxia either by greater release of adenosine or greater vascular sensitivity to it.

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Selected References

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