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. 1993 Jun;109(2):466–472. doi: 10.1111/j.1476-5381.1993.tb13592.x

Blockade by glibenclamide of the flow-evoked endothelial release of ATP that contributes to vasodilatation in the pulmonary vascular bed of the rat.

H Hasséssian 1, P Bodin 1, G Burnstock 1
PMCID: PMC2175668  PMID: 8358546

Abstract

1. The effect of step augmentation of flow rate on the level of adenosine -5'-triphosphate (ATP) measured in the Krebs perfusate was investigated, and the effect of glibenclamide on the release of ATP was tested in the rat pulmonary vascular bed. 2. For flow rates between 10.38 +/- 1.18 and 28.88 +/- 2.08 ml min-1 (n = 8) 1 microM suramin, a P2-purinoceptor antagonist, significantly (P < 0.05) increased vascular resistance under conditions of step augmentation of flow rate. This suggests that endogenous ATP released during increases in flow rate dilates pulmonary vessels. 3. In response to a step augmentation in flow rate from 9.13 +/- 0.97 to 18.3 +/- 1.69 ml min-1 (n = 4) ATP levels were up to 23 fold higher (P < 0.05) for 15 s, and gradually dropped to a level of about half the initial rise. Once the ATP levels had stabilized, another step augmentation of flow rate to 27.00 +/- 3.49 ml min-1 was able to evoke a corresponding increase of ATP release. The ability of the vascular bed to respond with increased ATP release after the initial ATP responses had tapered, demonstrates that the drop in ATP levels after the initial rise is not due to depletion of ATP. Furthermore, the maximal ATP response directly precedes the vasodilatation observed following each jump in perfusion pressure produced with each step increase in flow rate.(ABSTRACT TRUNCATED AT 250 WORDS)

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Selected References

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