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Article: Evidence for control of adenosine metabolism in rat oxidative skeletal muscle by changes in pH

TitleEvidence for control of adenosine metabolism in rat oxidative skeletal muscle by changes in pH
Authors
Issue Date2000
PublisherWiley-Blackwell Publishing Ltd.. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=0022-3751
Citation
Journal Of Physiology, 2000, v. 522 n. 3, p. 467-477 How to Cite?
Abstract1. We investigated the effects of pH elevation or depression on adenosine output from buffer-perfused rat gracilis muscle, and kinetic properties of adenosine-forming enzymes, 5'-nucleotidase (5'N) and non-specific phosphatase (PT), and adenosine-removing enzymes, adenosine kinase (AK) and adenosine deaminase (AD), in homogenates of muscle. 2. Depression of the perfusion buffer pH from 7.4 to 6.8, by addition of sodium acetate, reduced arterial perfusion pressure from 8.44 ± 1.44 to 7.33 ± 0.58 kPa, and increased adenosine output from 35 ± 5 to 56 ± 6 pmol min-1 (g wet wt muscle)-1 and AMP output from 1.8 ± 0.3 to 9.1 ± 3.9 pmol min-1 (g wet wt muscle)-1. 3. Elevation of the buffer pH to 7.8, by addition of ammonium chloride, reduced arterial perfusion pressure from 8.74 ± 0.57 to 6.96 ± 1.37 kPa, and increased adenosine output from 25 ± 5 to 47 ± 8 pmol min-1 (g wet wt muscle)-1 and AMP output from 3.7 ± 1.1 to 24.6 ± 6.8 pmol min-1 (g wet wt muscle)-1. 4. Activity of membrane-bound 5'N was an order of magnitude higher than that of either cytosolic 5'N or PT: pH depression reduced the K(m) of 5'N, which increased its capacity to form adenosine by 10-20% for every 0.5 unit decrease in pH within the physiological range. PT was only found in the membrane fraction: its contribution to extracellular adenosine formation increased from about 5% at pH 7.0 to about 15% at pH 8.0. 5. Cytosolic 5'N had a low activity, which was unaffected by pH; the rate of intracellular adenosine formation was an order of magnitude lower than the rate of adenosine removal by adenosine kinase or adenosine deaminase, which were both exclusively intracellular enzymes. 6. We conclude that (i) adenosine is formed in the extracellular compartment of rat skeletal muscle, principally by membrane-bound 5'N, where it is protected from enzymatic breakdown; (ii) adenosine is formed intracellularly at a very low rate, and is unlikely to leave the cell; (iii) enhanced adenosine formation at low pH is driven by an increased extracellular AMP concentration and an increased affinity of membrane-bound 5'N for AMP; (iv) enhanced adenosine formation at high pH is driven solely by the elevated extracellular AMP concentration, since the catalytic capacity of membrane 5'N is reduced at high pH.
Persistent Identifierhttp://hdl.handle.net/10722/49302
ISSN
2015 Impact Factor: 4.731
2015 SCImago Journal Rankings: 2.670
PubMed Central ID
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorCheng, Ben_HK
dc.contributor.authorEssackjee, HCen_HK
dc.contributor.authorBallard, HJen_HK
dc.date.accessioned2008-06-12T06:38:54Z-
dc.date.available2008-06-12T06:38:54Z-
dc.date.issued2000en_HK
dc.identifier.citationJournal Of Physiology, 2000, v. 522 n. 3, p. 467-477en_HK
dc.identifier.issn0022-3751en_HK
dc.identifier.urihttp://hdl.handle.net/10722/49302-
dc.description.abstract1. We investigated the effects of pH elevation or depression on adenosine output from buffer-perfused rat gracilis muscle, and kinetic properties of adenosine-forming enzymes, 5'-nucleotidase (5'N) and non-specific phosphatase (PT), and adenosine-removing enzymes, adenosine kinase (AK) and adenosine deaminase (AD), in homogenates of muscle. 2. Depression of the perfusion buffer pH from 7.4 to 6.8, by addition of sodium acetate, reduced arterial perfusion pressure from 8.44 ± 1.44 to 7.33 ± 0.58 kPa, and increased adenosine output from 35 ± 5 to 56 ± 6 pmol min-1 (g wet wt muscle)-1 and AMP output from 1.8 ± 0.3 to 9.1 ± 3.9 pmol min-1 (g wet wt muscle)-1. 3. Elevation of the buffer pH to 7.8, by addition of ammonium chloride, reduced arterial perfusion pressure from 8.74 ± 0.57 to 6.96 ± 1.37 kPa, and increased adenosine output from 25 ± 5 to 47 ± 8 pmol min-1 (g wet wt muscle)-1 and AMP output from 3.7 ± 1.1 to 24.6 ± 6.8 pmol min-1 (g wet wt muscle)-1. 4. Activity of membrane-bound 5'N was an order of magnitude higher than that of either cytosolic 5'N or PT: pH depression reduced the K(m) of 5'N, which increased its capacity to form adenosine by 10-20% for every 0.5 unit decrease in pH within the physiological range. PT was only found in the membrane fraction: its contribution to extracellular adenosine formation increased from about 5% at pH 7.0 to about 15% at pH 8.0. 5. Cytosolic 5'N had a low activity, which was unaffected by pH; the rate of intracellular adenosine formation was an order of magnitude lower than the rate of adenosine removal by adenosine kinase or adenosine deaminase, which were both exclusively intracellular enzymes. 6. We conclude that (i) adenosine is formed in the extracellular compartment of rat skeletal muscle, principally by membrane-bound 5'N, where it is protected from enzymatic breakdown; (ii) adenosine is formed intracellularly at a very low rate, and is unlikely to leave the cell; (iii) enhanced adenosine formation at low pH is driven by an increased extracellular AMP concentration and an increased affinity of membrane-bound 5'N for AMP; (iv) enhanced adenosine formation at high pH is driven solely by the elevated extracellular AMP concentration, since the catalytic capacity of membrane 5'N is reduced at high pH.en_HK
dc.format.extent388 bytes-
dc.format.mimetypetext/html-
dc.languageengen_HK
dc.publisherWiley-Blackwell Publishing Ltd.. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=0022-3751en_HK
dc.relation.ispartofJournal of Physiologyen_HK
dc.rightsThe Journal of Physiology. Copyright © Blackwell Publishing Ltd.en_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.rightsThe definitive version is available at www.blackwell-synergy.comen_HK
dc.subject.meshAdenosine - metabolismen_HK
dc.subject.meshMuscle, Skeletal - blood supply - enzymologyen_HK
dc.subject.meshOxidative Phosphorylationen_HK
dc.subject.meshPerfusionen_HK
dc.subject.meshPhosphoric Monoester Hydrolases - metabolismen_HK
dc.titleEvidence for control of adenosine metabolism in rat oxidative skeletal muscle by changes in pHen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0022-3751&volume=522&issue=3&spage=467&epage=477&date=2000&atitle=Evidence+for+control+of+adenosine+metabolism+in+rat+oxidative+skeletal+muscle+by+changes+in+pHen_HK
dc.identifier.emailBallard, HJ: ballard@hkucc.hku.hken_HK
dc.identifier.authorityBallard, HJ=rp00367en_HK
dc.description.naturepublished_or_final_versionen_HK
dc.identifier.doi10.1111/j.1469-7793.2000.t01-1-00467.xen_HK
dc.identifier.pmid10713970-
dc.identifier.pmcidPMC2269774en_HK
dc.identifier.scopuseid_2-s2.0-0034141741en_HK
dc.identifier.hkuros53111-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0034141741&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume522en_HK
dc.identifier.issue3en_HK
dc.identifier.spage467en_HK
dc.identifier.epage477en_HK
dc.identifier.isiWOS:000085537000011-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridCheng, B=21645039300en_HK
dc.identifier.scopusauthoridEssackjee, HC=6507657423en_HK
dc.identifier.scopusauthoridBallard, HJ=7005286310en_HK

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