Prostaglandin- and theophylline-induced Cl secretion in rat distal colon is inhibited by microtubule inhibitors
dc.contributor.author | Grotmol, T. | en_US |
dc.contributor.author | Dyke, R. W. | en_US |
dc.date.accessioned | 2006-09-11T14:45:58Z | |
dc.date.available | 2006-09-11T14:45:58Z | |
dc.date.issued | 1992-11 | en_US |
dc.identifier.citation | Grotmol, T.; Dyke, R. W.; (1992). "Prostaglandin- and theophylline-induced Cl secretion in rat distal colon is inhibited by microtubule inhibitors." Digestive Diseases and Sciences 37(11): 1709-1717. <http://hdl.handle.net/2027.42/44414> | en_US |
dc.identifier.issn | 0163-2116 | en_US |
dc.identifier.issn | 1573-2568 | en_US |
dc.identifier.uri | https://hdl.handle.net/2027.42/44414 | |
dc.identifier.uri | http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=1425071&dopt=citation | en_US |
dc.description.abstract | The aim of the present study was to examine the possible role of microtubules in chloride secretion by distal rat colon stimulated by prostaglandin (PGE 2 ) and theophylline. Distal colonic tissue from male rats was mounted in Ussing chambers, and short-circuit current (I sc ) was measured to assess chloride secretion. Three microtubule inhibitors, colchicine, nocodazole, and taxol, all inhibited the stimulated I sc and reduced the 60-min integrated secretory response to PGE 2 and theophylline (▪I sc dt) by 39–52%, whereas the inactive colchicine analog lumicolchicine did not. Atropine and tetrodotoxin had no effect on stimulated chloride secretion. To confirm the source of I sc , unidirectional 22 Na + and 36 Cl − fluxes were measured in tissues exposed to lumicolchicine (control) or colchicine. Control tissues absorbed both chloride [5.0 (1.1–8.6) (median and 95% confidence interval) μeq/cm 2 /hr] and sodium [2.8 (0.9–7.2) μeq/cm 2 /hr], and this net absorption was reduced by 96% and 79%, respectively, by treatment with PGE 2 and theophylline due to an increase in serosal-to-mucosal chloride and sodium movement. Colchicine-treated tissues exhibited similar net basal chloride and sodium absorption that was reduced by 71% and 75%, respectively, by treatment with PGE 2 and theophylline. Thus the PGE 2 - and theophylline-induced increase in chloride secretion was significantly reduced by colchicine ( P <0.05 by Wilcoxon rank-sum test), whereas colchicine had no effect on PGE 2 - and theophylline-induced changes in sodium fluxes. Furthermore, the colchinine-related changes in stimulated chloride secretion were numerically similar to colchicine-related changes in stimulated I sc . These findings indicate that microtubules are required for normal PGE 2 - and theophylline-induced chloride secretion in distal rat colon and suggest that induced chloride secretion may involve vesicular insertion of ion transporters into the plasma membrane or other microtubule-dependent regulatory processes. | en_US |
dc.format.extent | 967152 bytes | |
dc.format.extent | 3115 bytes | |
dc.format.mimetype | application/pdf | |
dc.format.mimetype | text/plain | |
dc.language.iso | en_US | |
dc.publisher | Kluwer Academic Publishers-Plenum Publishers; Plenum Publishing Corporation ; Springer Science+Business Media | en_US |
dc.subject.other | Gastroenterology | en_US |
dc.subject.other | Ussing Chamber | en_US |
dc.subject.other | Biochemistry, General | en_US |
dc.subject.other | Medicine & Public Health | en_US |
dc.subject.other | Hepatology | en_US |
dc.subject.other | Oncology | en_US |
dc.subject.other | Transplant Surgery | en_US |
dc.subject.other | Theophylline | en_US |
dc.subject.other | Intestinal Ion Transport | en_US |
dc.subject.other | Colchicine | en_US |
dc.subject.other | Radioisotopes | en_US |
dc.subject.other | Chloride Secretion | en_US |
dc.title | Prostaglandin- and theophylline-induced Cl secretion in rat distal colon is inhibited by microtubule inhibitors | en_US |
dc.type | Article | en_US |
dc.subject.hlbsecondlevel | Internal Medicine and Specialties | en_US |
dc.subject.hlbtoplevel | Health Sciences | en_US |
dc.description.peerreviewed | Peer Reviewed | en_US |
dc.contributor.affiliationum | Department of Medicine and Liver Center, University of California, 94143, San Francisco, California; University of Michigan, 1150 W. Medical Ctr. Dr., 6520 B MSRB-I Box 0682, 48109-0682, Ann Arbor, Michigan | en_US |
dc.contributor.affiliationother | Department of Medicine and Liver Center, University of California, 94143, San Francisco, California; Department of Tissue Culture, Institute for Cancer Research, The Norwegian Radium Hospital, N-0310, Oslo 3, Norway | en_US |
dc.contributor.affiliationumcampus | Ann Arbor | en_US |
dc.identifier.pmid | 1425071 | en_US |
dc.description.bitstreamurl | http://deepblue.lib.umich.edu/bitstream/2027.42/44414/1/10620_2005_Article_BF01299864.pdf | en_US |
dc.identifier.doi | http://dx.doi.org/10.1007/BF01299864 | en_US |
dc.identifier.source | Digestive Diseases and Sciences | en_US |
dc.owningcollname | Interdisciplinary and Peer-Reviewed |
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