File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Conference Paper: ATP breakdown rate does not control output of adenosine from contracting buffer-perfused rat gracilis muscle

TitleATP breakdown rate does not control output of adenosine from contracting 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. 17, abstract no. 66 How to Cite?
AbstractAdenosine is released from skeletal muscle during contractions and contributes to exercise hyperemia, but the mechanism(s) that control the adenosine production and release remain unclear. Adenosine is derived from adenosine triphosphate (ATP) breakdown, and the rate of ATP breakdown varies, depending on the conditions for the contraction (such as velocity of shortening, muscle length, etc). In this study, we investigate the influence of the rate of ATP breakdown, modified by varying the conditions under which the muscle contracts, on the adenosine output from the perfused rat gracilis muscle in-situ. The muscle was vascularly isolated and perfused at a constant flow rate of 40-50 pl/min/g, via a muscular branch of the femoral artery, with Kreb’s bicarbonate buffer (pH 7.3-7.4), supplemented with dextran and albumin, and equilibrated against 95% 02 / 5% COZ. ATP breakdown rate was varied by altering either the length of the muscle during isometric contractions or the weight lifted during isotonic contractions. Samples of venous effluent were collected before (control) and during supramaximal electrical stimulation (2 Hz) of the muscle via electrodes placed directly on its surface. Samples were purified by organic extraction, and their adenosine concentrations were determined by reversed-phase high-performance liquid chromatography. Under isometric c conditions, muscle contractions increased venous adenosine from 30 + 9 to 1473 f 3 18 nM (n = 12; PC 0.001 Student’s t-test), but neither resting nor stimulated adenosine output was affected by reducing muscle length to 10% below 1, (the length giving maximal active tension), although both passive and active tensions were decreased to 50%. Under isotonic conditions, stimulation increased venous adenosine from 428 + 55 nM to 19 12 + 28 1 nM (n = 12; P < O.OOO 1 ), but adenosine output was not influenced by the weight lifted by the muscle (either log, equivalent to the passive tension exhibited by the muscle when stretched to 1,, or 5g). Also, the change in venous adenosine due to muscle contractions (stimulation venous-control venous) was similar for both isotonic and isometric contractions. These data suggest that the rate of ATP breakdown by a contracting muscle may not be a major influence on the output of its vasoactive breakdown product, adenosine.
DescriptionSession - Purines: Release and Metabolism
Persistent Identifierhttp://hdl.handle.net/10722/105244
ISSN
2015 Impact Factor: 0.984

 

DC FieldValueLanguage
dc.contributor.authorEssackjee, HC-
dc.contributor.authorBallard, HJ-
dc.date.accessioned2010-09-25T22:26:03Z-
dc.date.available2010-09-25T22:26:03Z-
dc.date.issued1998-
dc.identifier.citationDrug Development Research, 1998, v. 43 n. 1, p. 17, abstract no. 66-
dc.identifier.issn0272-4391-
dc.identifier.urihttp://hdl.handle.net/10722/105244-
dc.descriptionSession - Purines: Release and Metabolism-
dc.description.abstractAdenosine is released from skeletal muscle during contractions and contributes to exercise hyperemia, but the mechanism(s) that control the adenosine production and release remain unclear. Adenosine is derived from adenosine triphosphate (ATP) breakdown, and the rate of ATP breakdown varies, depending on the conditions for the contraction (such as velocity of shortening, muscle length, etc). In this study, we investigate the influence of the rate of ATP breakdown, modified by varying the conditions under which the muscle contracts, on the adenosine output from the perfused rat gracilis muscle in-situ. The muscle was vascularly isolated and perfused at a constant flow rate of 40-50 pl/min/g, via a muscular branch of the femoral artery, with Kreb’s bicarbonate buffer (pH 7.3-7.4), supplemented with dextran and albumin, and equilibrated against 95% 02 / 5% COZ. ATP breakdown rate was varied by altering either the length of the muscle during isometric contractions or the weight lifted during isotonic contractions. Samples of venous effluent were collected before (control) and during supramaximal electrical stimulation (2 Hz) of the muscle via electrodes placed directly on its surface. Samples were purified by organic extraction, and their adenosine concentrations were determined by reversed-phase high-performance liquid chromatography. Under isometric c conditions, muscle contractions increased venous adenosine from 30 + 9 to 1473 f 3 18 nM (n = 12; PC 0.001 Student’s t-test), but neither resting nor stimulated adenosine output was affected by reducing muscle length to 10% below 1, (the length giving maximal active tension), although both passive and active tensions were decreased to 50%. Under isotonic conditions, stimulation increased venous adenosine from 428 + 55 nM to 19 12 + 28 1 nM (n = 12; P < O.OOO 1 ), but adenosine output was not influenced by the weight lifted by the muscle (either log, equivalent to the passive tension exhibited by the muscle when stretched to 1,, or 5g). Also, the change in venous adenosine due to muscle contractions (stimulation venous-control venous) was similar for both isotonic and isometric contractions. These data suggest that the rate of ATP breakdown by a contracting muscle may not be a major influence on the output of its vasoactive breakdown product, adenosine.-
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.titleATP breakdown rate does not control output of adenosine from contracting 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=17&epage=&date=1998&atitle=ATP+breakdown+rate+does+not+control+output+of+adenosine+from+contracting+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.hkuros37038-
dc.identifier.volume43-
dc.identifier.issue1-
dc.identifier.spage17, abstract no. 66-
dc.identifier.epage17, abstract no. 66-
dc.publisher.placeUnited States-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats