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Conference Paper: The effects of pH depression on the adenosine output from the in-situ buffer-perfused rat gracilis muscle

TitleThe effects of pH depression on the adenosine output from the in-situ buffer-perfused rat gracilis muscle
Authors
Issue Date1998
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/34597
Citation
Drug Development Research, 1998, v. 43 n. 1, p. 16, abstract no. 62 How to Cite?
AbstractIn-vivo studies showed that adenosine output increased with the depression of pH during either muscle contractions or acid infusion. However, the effect of pH elevation on adenosine output has never been reported. Several enzymes may be involved in the adenosine production from AMP, namely 5’-nucleotidase and the non-specific phosphatases, including alkaline phosphatase. The contribution of these enzymes to the adenosine production may vary at different pH values. We tested the effect of depression or elevation of pH on the adenosine output from rat gracilis muscle. The vascularly-isolated muscle was perfused in-situ at a constant flow rate of 40-50 pl/min/g. The pH of the perfusion buffer (Kreb’s-bicarbonate equilibrated against 95% 02 / 5% COZ, 37°C) was either depressed to 6.8 or elevated to 7.8 by substituting 30 mM sodium chloride with a similar concentration of sodium acetate or ammonium chloride, respectively. The vascularly isolated muscle was stretched to its resting length (1,) and perfused via a muscular branch of the femoral artery with buffer at pH 7.4 (control) and thereafter with buffer either at pH 6.8 (acidosis) or at pH 7.8 (alkalosis). Samples of venous effluent collected during both control and acidosis or alkalosis were purified by organic extraction and their adenosine concentrations were determined by reversed-phase high-performance liquid chromatography. Acidosis increased the venous adenosine concentration from 784 + 167 to 1170 + 263 nM (n=6; PcO.02 Student’s t-test); however, alkalosis did not significantly alter the venous adenosine (595 f 3 18 nM in control and 763 + 191 nM in alkalosis). Adenosine formation by 5’-nucleotidase increases at low pH, which may account for the enhanced adenosine production in acidosis. At elevated pH the adenosine formation by 5’- nucleotidase decreases, whereas the formation by alkaline phosphatase increases. These data suggest that the overall rate of adenosine production does not change with moderate elevation of pH. We speculate that the relative contributions of 5’-nucleotidase and alkaline phosphatase to the adenosine production may change as the pH increases.
DescriptionSession - Purines: Release and Metabolism
Persistent Identifierhttp://hdl.handle.net/10722/105077
ISSN
2015 Impact Factor: 0.984

 

DC FieldValueLanguage
dc.contributor.authorBallard, HJ-
dc.contributor.authorEssackjee, HC-
dc.date.accessioned2010-09-25T22:19:16Z-
dc.date.available2010-09-25T22:19:16Z-
dc.date.issued1998-
dc.identifier.citationDrug Development Research, 1998, v. 43 n. 1, p. 16, abstract no. 62-
dc.identifier.issn0272-4391-
dc.identifier.urihttp://hdl.handle.net/10722/105077-
dc.descriptionSession - Purines: Release and Metabolism-
dc.description.abstractIn-vivo studies showed that adenosine output increased with the depression of pH during either muscle contractions or acid infusion. However, the effect of pH elevation on adenosine output has never been reported. Several enzymes may be involved in the adenosine production from AMP, namely 5’-nucleotidase and the non-specific phosphatases, including alkaline phosphatase. The contribution of these enzymes to the adenosine production may vary at different pH values. We tested the effect of depression or elevation of pH on the adenosine output from rat gracilis muscle. The vascularly-isolated muscle was perfused in-situ at a constant flow rate of 40-50 pl/min/g. The pH of the perfusion buffer (Kreb’s-bicarbonate equilibrated against 95% 02 / 5% COZ, 37°C) was either depressed to 6.8 or elevated to 7.8 by substituting 30 mM sodium chloride with a similar concentration of sodium acetate or ammonium chloride, respectively. The vascularly isolated muscle was stretched to its resting length (1,) and perfused via a muscular branch of the femoral artery with buffer at pH 7.4 (control) and thereafter with buffer either at pH 6.8 (acidosis) or at pH 7.8 (alkalosis). Samples of venous effluent collected during both control and acidosis or alkalosis were purified by organic extraction and their adenosine concentrations were determined by reversed-phase high-performance liquid chromatography. Acidosis increased the venous adenosine concentration from 784 + 167 to 1170 + 263 nM (n=6; PcO.02 Student’s t-test); however, alkalosis did not significantly alter the venous adenosine (595 f 3 18 nM in control and 763 + 191 nM in alkalosis). Adenosine formation by 5’-nucleotidase increases at low pH, which may account for the enhanced adenosine production in acidosis. At elevated pH the adenosine formation by 5’- nucleotidase decreases, whereas the formation by alkaline phosphatase increases. These data suggest that the overall rate of adenosine production does not change with moderate elevation of pH. We speculate that the relative contributions of 5’-nucleotidase and alkaline phosphatase to the adenosine production may change as the pH increases.-
dc.languageeng-
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/34597-
dc.relation.ispartofDrug Development Research-
dc.rightsDrug Development Research. Copyright © John Wiley & Sons, Inc.-
dc.rightsPreprint: This is the pre-peer reviewed version of the following article: [FULL CITE], which has been published in final form at [Link to final article using the DOI]. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Self-Archiving. Postprint: This is the peer reviewed version of the following article: [FULL CITE], which has been published in final form at [Link to final article using the DOI]. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Self-Archiving. Special Statement for Preprint only Before publication: 'This is a preprint of an article accepted for publication in [The Journal of Pathology] Copyright © ([year]) ([Pathological Society of Great Britain and Ireland])'. After publication: the preprint notice should be amended to follows: 'This is a preprint of an article published in [include the complete citation information for the final version of the Contribution as published in the print edition of the Journal]' For Cochrane Library/ Cochrane Database of Systematic Reviews, add statement & acknowledgement : ‘This review is published as a Cochrane Review in the Cochrane Database of Systematic Reviews 20XX, Issue X. Cochrane Reviews are regularly updated as new evidence emerges and in response to comments and criticisms, and the Cochrane Database of Systematic Reviews should be consulted for the most recent version of the Review.’ Please include reference to the Review and hyperlink to the original version using the following format e.g. Authors. Title of Review. Cochrane Database of Systematic Reviews 20XX, Issue #. Art. No.: CD00XXXX. DOI: 10.1002/14651858.CD00XXXX (insert persistent link to the article by using the URL: http://dx.doi.org/10.1002/14651858.CD00XXXX) (This statement should refer to the most recent issue of the Cochrane Database of Systematic Reviews in which the Review published.)-
dc.titleThe effects of pH depression on the adenosine output from the in-situ buffer-perfused rat gracilis muscle-
dc.typeConference_Paper-
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0272-4391&volume=43&spage=16&epage=&date=1998&atitle=The+effects+of+pH+depression+on+the+adenosine+output+from+the+in-situ+buffer-perfused+rat+gracilis+muscleen_HK
dc.identifier.emailBallard, HJ: ballard@hkucc.hku.hk-
dc.identifier.authorityBallard, HJ=rp00367-
dc.identifier.doi10.1002/(SICI)1098-2299(199801)43:1<16::AID-DDR2>3.0.CO;2-T-
dc.identifier.hkuros37030-
dc.identifier.volume43-
dc.identifier.issue1-
dc.identifier.spage16, abstract no. 62-
dc.identifier.epage16, abstract no. 62-
dc.publisher.placeUnited States-

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