Mechanisms of Sodium Transport at the Blood-Brain Barrier Studied with In Situ Perfusion of Rat Brain
dc.contributor.author | Ren, Xiao-dan | en_US |
dc.contributor.author | Betz, A. Lorris | en_US |
dc.date.accessioned | 2010-04-01T15:13:12Z | |
dc.date.available | 2010-04-01T15:13:12Z | |
dc.date.issued | 1996-02 | en_US |
dc.identifier.citation | Ren, Xiao-dan; Betz, A. Lorris (1996). "Mechanisms of Sodium Transport at the Blood-Brain Barrier Studied with In Situ Perfusion of Rat Brain." Journal of Neurochemistry 66(2): 756-763. <http://hdl.handle.net/2027.42/65689> | en_US |
dc.identifier.issn | 0022-3042 | en_US |
dc.identifier.issn | 1471-4159 | en_US |
dc.identifier.uri | https://hdl.handle.net/2027.42/65689 | |
dc.identifier.uri | http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=8592149&dopt=citation | en_US |
dc.description.abstract | The mechanism of unidirectional transport of sodium from blood to brain in pentobarbital-anesthetized rats was examined using in situ perfusion. Sodium transport followed Michaelis-Menten saturation kinetics with a V max of 50.1 nmol/g/min and a K m of 17.7 m M in the left frontal cortex. The kinetic analysis indicated that, at a physiologic sodium concentration, ∼26% of sodium transport at the blood-brain barrier (BBB) was carrier mediated. Dimethylamiloride (25 µ M ), an inhibitor of Na + /H + exchange, reduced sodium transport by 28%, whereas phenamil (25 µ M ), a sodium channel inhibitor, reduced the transfer constant for sodium by 22%. Bumetanide (250 µ M ) and hydrochlorothiazide (1.5 m M ), inhibitors of Na + -K + -2Cl − /NaCl symport, were ineffective in reducing blood to brain sodium transport. Acetazolamide (0.25 m M ), an inhibitor of carbonic anhydrase, did not change sodium transport at the BBB. Finally, a perfusate pH of 7.0 or 7.8 or a perfusate Pco 2 of 86 mm Hg failed to change sodium transport. These results indicate that 50% of transcellular transport of sodium from blood to brain occurs through Na + /H + exchange and a sodium channel in the luminal membrane of the BBB. We propose that the sodium transport systems at the luminal membrane of the BBB, in conjunction with Cl − /HCO 3 − exchange, lead to net NaCl secretion and obligate water transport into the brain. | en_US |
dc.format.extent | 799120 bytes | |
dc.format.extent | 3110 bytes | |
dc.format.mimetype | application/pdf | |
dc.format.mimetype | text/plain | |
dc.publisher | Blackwell Science Ltd | en_US |
dc.rights | Blackwell Science Inc | en_US |
dc.subject.other | Brain | en_US |
dc.subject.other | Blood-brain Barrier | en_US |
dc.subject.other | Transport | en_US |
dc.subject.other | Sodium | en_US |
dc.subject.other | In Situ Perfusion | en_US |
dc.title | Mechanisms of Sodium Transport at the Blood-Brain Barrier Studied with In Situ Perfusion of Rat Brain | en_US |
dc.type | Article | en_US |
dc.rights.robots | IndexNoFollow | en_US |
dc.subject.hlbsecondlevel | Neurosciences | en_US |
dc.subject.hlbtoplevel | Health Sciences | en_US |
dc.description.peerreviewed | Peer Reviewed | en_US |
dc.contributor.affiliationum | † Pediatrics and Neurology, University of Michigan, Ann Arbor, Michigan, U.S.A. | en_US |
dc.identifier.pmid | 8592149 | en_US |
dc.description.bitstreamurl | http://deepblue.lib.umich.edu/bitstream/2027.42/65689/1/j.1471-4159.1996.66020756.x.pdf | |
dc.identifier.doi | 10.1046/j.1471-4159.1996.66020756.x | en_US |
dc.identifier.source | Journal of Neurochemistry | en_US |
dc.owningcollname | Interdisciplinary and Peer-Reviewed |
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