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. 1995 Feb;114(4):846–850. doi: 10.1111/j.1476-5381.1995.tb13281.x

Interacting roles of nitric oxide and ATP in the pulmonary circulation of the rat.

H Hasséssian 1, G Burnstock 1
PMCID: PMC1510219  PMID: 7773545

Abstract

1. The potentiating effect of NG-nitro-L-arginine methyl ester, (L-NAME) a nitric oxide synthesis inhibitor, on responses of the rat pulmonary vascular pressure (PVP) to purinoceptor agonists was examined. 2. At a constant flow of 23 ml min-1 the PVP was 22.4 +/- 2.5 mmHg (n = 15), and treatment with 100 microM L-NAME for 15 min was without effect on the PVP. After the tone was raised with 28 nmol 9,11-dideoxy-11 alpha, 9 alpha-epoxymethano-prostaglandin F2 alpha (U-46619), the PVP was 29.4 +/- 3.3 mmHg and treatment with 100 microM L-NAME was still without effect on the PVP. It appears that there is a graded release of nitric oxide in response to different levels of steady shear stress and in our experimental model the threshold for detection was not reached under basal conditions. 3. In contrast, when the circulation was challenged with 30 s step, additive increases in flow between 11 and 50 ml min-1 (n = 8), treatment with 100 microM L-NAME produced a significant (P < 0.05) increase in PVP suggesting that changes in flow-derived forces evoke the release of nitric oxide. This was evident for flow rates above 30 ml min-1. 4. In preparations in which tone was raised with U-46619, a dose of 1 x 10(-8) mol ATP or 2-meSATP evoked a drop in PVP while alpha,beta-meATP produced an increase in PVP under constant flow of 23 ml min-1. After treatment with 100 microM L-NAME, all three purinoceptor agonists evoked an increase in PVP.(ABSTRACT TRUNCATED AT 250 WORDS)

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Selected References

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