Complete intracellular pH protection during extracellular pH depression is associated with hypercarbia tolerance in white sturgeon, Acipenser transmontanus.
Identifieur interne : 000417 ( PubMed/Checkpoint ); précédent : 000416; suivant : 000418Complete intracellular pH protection during extracellular pH depression is associated with hypercarbia tolerance in white sturgeon, Acipenser transmontanus.
Auteurs : D W Baker [Canada] ; V. Matey ; K T Huynh ; J M Wilson ; J D Morgan ; C J BraunerSource :
- American journal of physiology. Regulatory, integrative and comparative physiology [ 0363-6119 ] ; 2009.
English descriptors
- KwdEn :
- Acid-Base Equilibrium, Acidosis, Respiratory (metabolism), Acidosis, Respiratory (pathology), Acidosis, Respiratory (physiopathology), Adaptation, Physiological, Animals, Bicarbonates (metabolism), Brain (metabolism), Carbon Dioxide (blood), Carbon Dioxide (metabolism), Chlorides (metabolism), Fishes, Gills (metabolism), Gills (physiopathology), Gills (ultrastructure), Hydrogen-Ion Concentration, Hypercapnia (metabolism), Hypercapnia (pathology), Hypercapnia (physiopathology), Liver (metabolism), Muscle Fibers, Fast-Twitch (metabolism), Myocardium (metabolism), Proton-Translocating ATPases (metabolism), Sodium-Potassium-Exchanging ATPase (metabolism), Time Factors.
- MESH :
- chemical , blood : Carbon Dioxide.
- chemical , metabolism : Bicarbonates, Carbon Dioxide, Chlorides, Proton-Translocating ATPases, Sodium-Potassium-Exchanging ATPase.
- metabolism : Acidosis, Respiratory, Brain, Gills, Hypercapnia, Liver, Muscle Fibers, Fast-Twitch, Myocardium.
- pathology : Acidosis, Respiratory, Hypercapnia.
- physiopathology : Acidosis, Respiratory, Gills, Hypercapnia.
- ultrastructure : Gills.
- Acid-Base Equilibrium, Adaptation, Physiological, Animals, Fishes, Hydrogen-Ion Concentration, Time Factors.
Abstract
Sturgeons are among the most CO2 tolerant of fishes investigated to date. However, the basis of this exceptional CO2 tolerance is unknown. Here, white sturgeon, Acipenser transmontanus, were exposed to elevated CO2 to investigate the mechanisms associated with short-term hypercarbia tolerance. During exposure to 1.5 kPa Pco2, transient blood pH [extracellular pH (pHe)] depression was compensated within 24 h and associated with net plasma HCO3- accumulation and equimolar Cl- loss, and changes in gill morphology, such as a decrease in apical surface area of mitochondrial-rich cells. These findings indicate that pHe recovery at this level of hypercarbia is accomplished in a manner similar to most freshwater teleost species studied to date, although branchial mechanisms involved may differ. White sturgeon exposed to more severe hypercarbia (3 and 6 kPa Pco2) for 48 h exhibited incomplete pH compensation in blood and red blood cells. Despite pHe depression, intracellular pH (pHi) of white muscle, heart, brain, and liver did not decrease during a transient (6 h of 1.5 kPa Pco2) or prolonged (48 h at 3 and 6 kPa Pco2 blood acidosis. This pHi protection was not due to high intrinsic buffering in tissues. Such tight active cellular regulation of pHi in the absence of pHe compensation represents a unique pattern for non-air-breathing fishes, and we hypothesize that it is the basis for the exceptional CO2 tolerance of white sturgeon and, likely, other CO2 tolerant fishes. Further research to elucidate the specific mechanisms responsible for this tremendous pH regulatory capacity in tissues of white sturgeon is warranted.
DOI: 10.1152/ajpregu.90767.2008
PubMed: 19339675
Affiliations:
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Matey</name></author><author><name sortKey="Huynh, K T" sort="Huynh, K T" uniqKey="Huynh K" first="K T" last="Huynh">K T Huynh</name></author><author><name sortKey="Wilson, J M" sort="Wilson, J M" uniqKey="Wilson J" first="J M" last="Wilson">J M Wilson</name></author><author><name sortKey="Morgan, J D" sort="Morgan, J D" uniqKey="Morgan J" first="J D" last="Morgan">J D Morgan</name></author><author><name sortKey="Brauner, C J" sort="Brauner, C J" uniqKey="Brauner C" first="C J" last="Brauner">C J Brauner</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2009">2009</date><idno type="RBID">pubmed:19339675</idno><idno type="pmid">19339675</idno><idno type="doi">10.1152/ajpregu.90767.2008</idno><idno type="wicri:Area/PubMed/Corpus">000428</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000428</idno><idno type="wicri:Area/PubMed/Curation">000428</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">000428</idno><idno type="wicri:Area/PubMed/Checkpoint">000428</idno><idno type="wicri:explorRef" wicri:stream="Checkpoint" wicri:step="PubMed">000428</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Complete intracellular pH protection during extracellular pH depression is associated with hypercarbia tolerance in white sturgeon, Acipenser transmontanus.</title><author><name sortKey="Baker, D W" sort="Baker, D W" uniqKey="Baker D" first="D W" last="Baker">D W Baker</name><affiliation wicri:level="1"><nlm:affiliation>Department of Zoology, University of British Columbia, Vancouver, British Columbia V6T 1Z4, Canada. baker@zoology.ubc.ca</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Department of Zoology, University of British Columbia, Vancouver, British Columbia V6T 1Z4</wicri:regionArea><wicri:noRegion>British Columbia V6T 1Z4</wicri:noRegion></affiliation></author><author><name sortKey="Matey, V" sort="Matey, V" uniqKey="Matey V" first="V" last="Matey">V. Matey</name></author><author><name sortKey="Huynh, K T" sort="Huynh, K T" uniqKey="Huynh K" first="K T" last="Huynh">K T Huynh</name></author><author><name sortKey="Wilson, J M" sort="Wilson, J M" uniqKey="Wilson J" first="J M" last="Wilson">J M Wilson</name></author><author><name sortKey="Morgan, J D" sort="Morgan, J D" uniqKey="Morgan J" first="J D" last="Morgan">J D Morgan</name></author><author><name sortKey="Brauner, C J" sort="Brauner, C J" uniqKey="Brauner C" first="C J" last="Brauner">C J Brauner</name></author></analytic><series><title level="j">American journal of physiology. Regulatory, integrative and comparative physiology</title><idno type="ISSN">0363-6119</idno><imprint><date when="2009" type="published">2009</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Acid-Base Equilibrium</term><term>Acidosis, Respiratory (metabolism)</term><term>Acidosis, Respiratory (pathology)</term><term>Acidosis, Respiratory (physiopathology)</term><term>Adaptation, Physiological</term><term>Animals</term><term>Bicarbonates (metabolism)</term><term>Brain (metabolism)</term><term>Carbon Dioxide (blood)</term><term>Carbon Dioxide (metabolism)</term><term>Chlorides (metabolism)</term><term>Fishes</term><term>Gills (metabolism)</term><term>Gills (physiopathology)</term><term>Gills (ultrastructure)</term><term>Hydrogen-Ion Concentration</term><term>Hypercapnia (metabolism)</term><term>Hypercapnia (pathology)</term><term>Hypercapnia (physiopathology)</term><term>Liver (metabolism)</term><term>Muscle Fibers, Fast-Twitch (metabolism)</term><term>Myocardium (metabolism)</term><term>Proton-Translocating ATPases (metabolism)</term><term>Sodium-Potassium-Exchanging ATPase (metabolism)</term><term>Time Factors</term></keywords><keywords scheme="MESH" type="chemical" qualifier="blood" xml:lang="en"><term>Carbon Dioxide</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Bicarbonates</term><term>Carbon Dioxide</term><term>Chlorides</term><term>Proton-Translocating ATPases</term><term>Sodium-Potassium-Exchanging ATPase</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Acidosis, Respiratory</term><term>Brain</term><term>Gills</term><term>Hypercapnia</term><term>Liver</term><term>Muscle Fibers, Fast-Twitch</term><term>Myocardium</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Acidosis, Respiratory</term><term>Hypercapnia</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Acidosis, Respiratory</term><term>Gills</term><term>Hypercapnia</term></keywords><keywords scheme="MESH" qualifier="ultrastructure" xml:lang="en"><term>Gills</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Acid-Base Equilibrium</term><term>Adaptation, Physiological</term><term>Animals</term><term>Fishes</term><term>Hydrogen-Ion Concentration</term><term>Time Factors</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Sturgeons are among the most CO2 tolerant of fishes investigated to date. However, the basis of this exceptional CO2 tolerance is unknown. Here, white sturgeon, Acipenser transmontanus, were exposed to elevated CO2 to investigate the mechanisms associated with short-term hypercarbia tolerance. During exposure to 1.5 kPa Pco2, transient blood pH [extracellular pH (pHe)] depression was compensated within 24 h and associated with net plasma HCO3- accumulation and equimolar Cl- loss, and changes in gill morphology, such as a decrease in apical surface area of mitochondrial-rich cells. These findings indicate that pHe recovery at this level of hypercarbia is accomplished in a manner similar to most freshwater teleost species studied to date, although branchial mechanisms involved may differ. White sturgeon exposed to more severe hypercarbia (3 and 6 kPa Pco2) for 48 h exhibited incomplete pH compensation in blood and red blood cells. Despite pHe depression, intracellular pH (pHi) of white muscle, heart, brain, and liver did not decrease during a transient (6 h of 1.5 kPa Pco2) or prolonged (48 h at 3 and 6 kPa Pco2 blood acidosis. This pHi protection was not due to high intrinsic buffering in tissues. Such tight active cellular regulation of pHi in the absence of pHe compensation represents a unique pattern for non-air-breathing fishes, and we hypothesize that it is the basis for the exceptional CO2 tolerance of white sturgeon and, likely, other CO2 tolerant fishes. Further research to elucidate the specific mechanisms responsible for this tremendous pH regulatory capacity in tissues of white sturgeon is warranted.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">19339675</PMID><DateCreated><Year>2009</Year><Month>05</Month><Day>21</Day></DateCreated><DateCompleted><Year>2009</Year><Month>07</Month><Day>02</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Print">0363-6119</ISSN><JournalIssue CitedMedium="Print"><Volume>296</Volume><Issue>6</Issue><PubDate><Year>2009</Year><Month>Jun</Month></PubDate></JournalIssue><Title>American journal of physiology. Regulatory, integrative and comparative physiology</Title><ISOAbbreviation>Am. J. Physiol. Regul. Integr. Comp. Physiol.</ISOAbbreviation></Journal><ArticleTitle>Complete intracellular pH protection during extracellular pH depression is associated with hypercarbia tolerance in white sturgeon, Acipenser transmontanus.</ArticleTitle><Pagination><MedlinePgn>R1868-80</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1152/ajpregu.90767.2008</ELocationID><Abstract><AbstractText>Sturgeons are among the most CO2 tolerant of fishes investigated to date. However, the basis of this exceptional CO2 tolerance is unknown. Here, white sturgeon, Acipenser transmontanus, were exposed to elevated CO2 to investigate the mechanisms associated with short-term hypercarbia tolerance. During exposure to 1.5 kPa Pco2, transient blood pH [extracellular pH (pHe)] depression was compensated within 24 h and associated with net plasma HCO3- accumulation and equimolar Cl- loss, and changes in gill morphology, such as a decrease in apical surface area of mitochondrial-rich cells. These findings indicate that pHe recovery at this level of hypercarbia is accomplished in a manner similar to most freshwater teleost species studied to date, although branchial mechanisms involved may differ. White sturgeon exposed to more severe hypercarbia (3 and 6 kPa Pco2) for 48 h exhibited incomplete pH compensation in blood and red blood cells. Despite pHe depression, intracellular pH (pHi) of white muscle, heart, brain, and liver did not decrease during a transient (6 h of 1.5 kPa Pco2) or prolonged (48 h at 3 and 6 kPa Pco2 blood acidosis. This pHi protection was not due to high intrinsic buffering in tissues. Such tight active cellular regulation of pHi in the absence of pHe compensation represents a unique pattern for non-air-breathing fishes, and we hypothesize that it is the basis for the exceptional CO2 tolerance of white sturgeon and, likely, other CO2 tolerant fishes. Further research to elucidate the specific mechanisms responsible for this tremendous pH regulatory capacity in tissues of white sturgeon is warranted.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Baker</LastName><ForeName>D W</ForeName><Initials>DW</Initials><AffiliationInfo><Affiliation>Department of Zoology, University of British Columbia, Vancouver, British Columbia V6T 1Z4, Canada. baker@zoology.ubc.ca</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Matey</LastName><ForeName>V</ForeName><Initials>V</Initials></Author><Author ValidYN="Y"><LastName>Huynh</LastName><ForeName>K T</ForeName><Initials>KT</Initials></Author><Author ValidYN="Y"><LastName>Wilson</LastName><ForeName>J M</ForeName><Initials>JM</Initials></Author><Author ValidYN="Y"><LastName>Morgan</LastName><ForeName>J D</ForeName><Initials>JD</Initials></Author><Author ValidYN="Y"><LastName>Brauner</LastName><ForeName>C J</ForeName><Initials>CJ</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2009</Year><Month>04</Month><Day>01</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Am J Physiol Regul Integr Comp Physiol</MedlineTA><NlmUniqueID>100901230</NlmUniqueID><ISSNLinking>0363-6119</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D001639">Bicarbonates</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D002712">Chlorides</NameOfSubstance></Chemical><Chemical><RegistryNumber>142M471B3J</RegistryNumber><NameOfSubstance UI="D002245">Carbon Dioxide</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.6.3.14</RegistryNumber><NameOfSubstance UI="D006180">Proton-Translocating ATPases</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.6.3.9</RegistryNumber><NameOfSubstance UI="D000254">Sodium-Potassium-Exchanging ATPase</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000136" MajorTopicYN="Y">Acid-Base Equilibrium</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000142" MajorTopicYN="N">Acidosis, Respiratory</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000222" MajorTopicYN="N">Adaptation, Physiological</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001639" MajorTopicYN="N">Bicarbonates</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001921" MajorTopicYN="N">Brain</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002245" MajorTopicYN="N">Carbon Dioxide</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002712" MajorTopicYN="N">Chlorides</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005399" MajorTopicYN="N">Fishes</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005880" MajorTopicYN="N">Gills</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName><QualifierName UI="Q000648" MajorTopicYN="N">ultrastructure</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006863" MajorTopicYN="N">Hydrogen-Ion Concentration</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006935" MajorTopicYN="N">Hypercapnia</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008099" MajorTopicYN="N">Liver</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018656" MajorTopicYN="N">Muscle Fibers, Fast-Twitch</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009206" MajorTopicYN="N">Myocardium</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006180" MajorTopicYN="N">Proton-Translocating ATPases</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000254" MajorTopicYN="N">Sodium-Potassium-Exchanging ATPase</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013997" MajorTopicYN="N">Time Factors</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2009</Year><Month>4</Month><Day>3</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2009</Year><Month>4</Month><Day>3</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2009</Year><Month>7</Month><Day>3</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">19339675</ArticleId><ArticleId IdType="pii">90767.2008</ArticleId><ArticleId IdType="doi">10.1152/ajpregu.90767.2008</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Canada</li></country></list><tree><noCountry><name sortKey="Brauner, C J" sort="Brauner, C J" uniqKey="Brauner C" first="C J" last="Brauner">C J Brauner</name><name sortKey="Huynh, K T" sort="Huynh, K T" uniqKey="Huynh K" first="K T" last="Huynh">K T Huynh</name><name sortKey="Matey, V" sort="Matey, V" uniqKey="Matey V" first="V" last="Matey">V. Matey</name><name sortKey="Morgan, J D" sort="Morgan, J D" uniqKey="Morgan J" first="J D" last="Morgan">J D Morgan</name><name sortKey="Wilson, J M" sort="Wilson, J M" uniqKey="Wilson J" first="J M" last="Wilson">J M Wilson</name></noCountry><country name="Canada"><noRegion><name sortKey="Baker, D W" sort="Baker, D W" uniqKey="Baker D" first="D W" last="Baker">D W Baker</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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