The Long-lasting Effect of TU-199, a Novel H+,K+-ATPase Inhibitor, on Gastric Acid Secretion in Dogs
We have used Heidenhain‐pouch dogs to investigate the effects of (±)‐5‐methoxy‐2‐{[(4‐methoxy‐3,5‐dimethylpyrid‐2‐yl)methyl]sulphinyl}‐1H‐imidazo[4,5‐b]pyridine (TU‐199), an imidazopyridine derivative, on gastric acid secretion stimulated by histamine, carbachol and tetragastrin. We have also invest...
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| Veröffentlicht in: | Journal of pharmacy and pharmacology 1999-04, Vol.51 (4), p.457-464 |
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| creator | UCHIYAMA, KAZUYUKI WAKATSUKI, DAISUKE KAKINOKI, BUNPEI TAKEUCHI, YOSHISHIGE ARAKI, TSUTOMU MORINAKA, YASUHIRO |
| description | We have used Heidenhain‐pouch dogs to investigate the effects of (±)‐5‐methoxy‐2‐{[(4‐methoxy‐3,5‐dimethylpyrid‐2‐yl)methyl]sulphinyl}‐1H‐imidazo[4,5‐b]pyridine (TU‐199), an imidazopyridine derivative, on gastric acid secretion stimulated by histamine, carbachol and tetragastrin. We have also investigated the duration of the antisecretory effect of TU‐199 using a measurement of intragastric pH for 24 h in gastric fistula dogs whose gastric acid secretion was stimulated by histamine.
Single oral administration of TU‐199 (0.1, 0.2 and 0.4 mg kg−1) dose‐dependently suppressed gastric acid secretion stimulated by histamine infusion. Oral treatment with TU‐199 (0.2, 0.4 and 0.8 mg kg−1) also dose‐dependently inhibited acid secretion induced by carbachol and tetragastrin. The inhibitory effect of TU‐199 on stimulated gastric acid secretion was more potent than that of omeprazole, a well‐known H+,K+‐ATPase inhibitor in dogs. Repeated oral treatment with TU‐199 at a dose of 0.2 mg kg−1 once a day for seven days markedly suppressed histamine‐stimulated gastric acid secretion in dogs. This inhibitory effect of TU‐199 reached a maximum level after three or four doses and was more pronounced than that of omeprazole or lansoprazole. In gastric fistula dogs, the duration of intragastric pH‐elevation by administration of TU‐199 (0.3 mg kg−1) was much longer than that of omeprazole (0.6 mg kg−1) or lansoprazole (0.9 mg kg−1). The IC50 values (doses resulting in 50% inhibition) of TU‐199, omeprazole and lansoprazole with regard to H+,K+‐ATPase activity in dog gastric mucosal microsomes were 8.6, 8.8 and 9.9 μM, respectively.
These results indicate that TU‐199 inhibits gastric acid secretion via suppression of a H+,K+‐ATPase activity. Our findings also suggest that TU‐199 might have potent and long‐lasting effects on gastric acid secretion. |
| doi_str_mv | 10.1211/0022357991772510 |
| format | Article |
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Single oral administration of TU‐199 (0.1, 0.2 and 0.4 mg kg−1) dose‐dependently suppressed gastric acid secretion stimulated by histamine infusion. Oral treatment with TU‐199 (0.2, 0.4 and 0.8 mg kg−1) also dose‐dependently inhibited acid secretion induced by carbachol and tetragastrin. The inhibitory effect of TU‐199 on stimulated gastric acid secretion was more potent than that of omeprazole, a well‐known H+,K+‐ATPase inhibitor in dogs. Repeated oral treatment with TU‐199 at a dose of 0.2 mg kg−1 once a day for seven days markedly suppressed histamine‐stimulated gastric acid secretion in dogs. This inhibitory effect of TU‐199 reached a maximum level after three or four doses and was more pronounced than that of omeprazole or lansoprazole. In gastric fistula dogs, the duration of intragastric pH‐elevation by administration of TU‐199 (0.3 mg kg−1) was much longer than that of omeprazole (0.6 mg kg−1) or lansoprazole (0.9 mg kg−1). The IC50 values (doses resulting in 50% inhibition) of TU‐199, omeprazole and lansoprazole with regard to H+,K+‐ATPase activity in dog gastric mucosal microsomes were 8.6, 8.8 and 9.9 μM, respectively.
These results indicate that TU‐199 inhibits gastric acid secretion via suppression of a H+,K+‐ATPase activity. Our findings also suggest that TU‐199 might have potent and long‐lasting effects on gastric acid secretion.</description><identifier>ISSN: 0022-3573</identifier><identifier>EISSN: 2042-7158</identifier><identifier>DOI: 10.1211/0022357991772510</identifier><identifier>PMID: 10385219</identifier><identifier>CODEN: JPPMAB</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>2-Pyridinylmethylsulfinylbenzimidazoles ; Analgesics, Non-Narcotic - pharmacology ; Animals ; Anti-Ulcer Agents - pharmacology ; Biological and medical sciences ; Carbachol - pharmacology ; Digestive system ; Dogs ; Dose-Response Relationship, Drug ; Enzyme Inhibitors - pharmacology ; Female ; Gastric Acid - metabolism ; Gastric Fistula ; Gastric Mucosa - drug effects ; Gastric Mucosa - enzymology ; Gastric Mucosa - metabolism ; H(+)-K(+)-Exchanging ATPase - metabolism ; Histamine - pharmacology ; Hydrogen-Ion Concentration ; Imidazoles - pharmacology ; Lansoprazole ; Male ; Medical sciences ; Microsomes - drug effects ; Microsomes - enzymology ; Omeprazole - analogs & derivatives ; Omeprazole - pharmacology ; Pharmacology. Drug treatments ; Proton Pump Inhibitors ; Pyridines - pharmacology ; Stomach - drug effects ; Stomach - surgery ; Tetragastrin - pharmacology ; Time Factors</subject><ispartof>Journal of pharmacy and pharmacology, 1999-04, Vol.51 (4), p.457-464</ispartof><rights>1999 Royal Pharmaceutical Society of Great Britain</rights><rights>1999 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4506-28501727008e88ab3949704971823cbf6875eef1e2996811887ff73cd5e8e1463</citedby><cites>FETCH-LOGICAL-c4506-28501727008e88ab3949704971823cbf6875eef1e2996811887ff73cd5e8e1463</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1211%2F0022357991772510$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1211%2F0022357991772510$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1798336$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10385219$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>UCHIYAMA, KAZUYUKI</creatorcontrib><creatorcontrib>WAKATSUKI, DAISUKE</creatorcontrib><creatorcontrib>KAKINOKI, BUNPEI</creatorcontrib><creatorcontrib>TAKEUCHI, YOSHISHIGE</creatorcontrib><creatorcontrib>ARAKI, TSUTOMU</creatorcontrib><creatorcontrib>MORINAKA, YASUHIRO</creatorcontrib><title>The Long-lasting Effect of TU-199, a Novel H+,K+-ATPase Inhibitor, on Gastric Acid Secretion in Dogs</title><title>Journal of pharmacy and pharmacology</title><addtitle>J Pharm Pharmacol</addtitle><description>We have used Heidenhain‐pouch dogs to investigate the effects of (±)‐5‐methoxy‐2‐{[(4‐methoxy‐3,5‐dimethylpyrid‐2‐yl)methyl]sulphinyl}‐1H‐imidazo[4,5‐b]pyridine (TU‐199), an imidazopyridine derivative, on gastric acid secretion stimulated by histamine, carbachol and tetragastrin. We have also investigated the duration of the antisecretory effect of TU‐199 using a measurement of intragastric pH for 24 h in gastric fistula dogs whose gastric acid secretion was stimulated by histamine.
Single oral administration of TU‐199 (0.1, 0.2 and 0.4 mg kg−1) dose‐dependently suppressed gastric acid secretion stimulated by histamine infusion. Oral treatment with TU‐199 (0.2, 0.4 and 0.8 mg kg−1) also dose‐dependently inhibited acid secretion induced by carbachol and tetragastrin. The inhibitory effect of TU‐199 on stimulated gastric acid secretion was more potent than that of omeprazole, a well‐known H+,K+‐ATPase inhibitor in dogs. Repeated oral treatment with TU‐199 at a dose of 0.2 mg kg−1 once a day for seven days markedly suppressed histamine‐stimulated gastric acid secretion in dogs. This inhibitory effect of TU‐199 reached a maximum level after three or four doses and was more pronounced than that of omeprazole or lansoprazole. In gastric fistula dogs, the duration of intragastric pH‐elevation by administration of TU‐199 (0.3 mg kg−1) was much longer than that of omeprazole (0.6 mg kg−1) or lansoprazole (0.9 mg kg−1). The IC50 values (doses resulting in 50% inhibition) of TU‐199, omeprazole and lansoprazole with regard to H+,K+‐ATPase activity in dog gastric mucosal microsomes were 8.6, 8.8 and 9.9 μM, respectively.
These results indicate that TU‐199 inhibits gastric acid secretion via suppression of a H+,K+‐ATPase activity. Our findings also suggest that TU‐199 might have potent and long‐lasting effects on gastric acid secretion.</description><subject>2-Pyridinylmethylsulfinylbenzimidazoles</subject><subject>Analgesics, Non-Narcotic - pharmacology</subject><subject>Animals</subject><subject>Anti-Ulcer Agents - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Carbachol - pharmacology</subject><subject>Digestive system</subject><subject>Dogs</subject><subject>Dose-Response Relationship, Drug</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>Female</subject><subject>Gastric Acid - metabolism</subject><subject>Gastric Fistula</subject><subject>Gastric Mucosa - drug effects</subject><subject>Gastric Mucosa - enzymology</subject><subject>Gastric Mucosa - metabolism</subject><subject>H(+)-K(+)-Exchanging ATPase - metabolism</subject><subject>Histamine - pharmacology</subject><subject>Hydrogen-Ion Concentration</subject><subject>Imidazoles - pharmacology</subject><subject>Lansoprazole</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Microsomes - drug effects</subject><subject>Microsomes - enzymology</subject><subject>Omeprazole - analogs & derivatives</subject><subject>Omeprazole - pharmacology</subject><subject>Pharmacology. Drug treatments</subject><subject>Proton Pump Inhibitors</subject><subject>Pyridines - pharmacology</subject><subject>Stomach - drug effects</subject><subject>Stomach - surgery</subject><subject>Tetragastrin - pharmacology</subject><subject>Time Factors</subject><issn>0022-3573</issn><issn>2042-7158</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkE1vEzEQhi0EoqFw54R8QFwagz_WX8eotEkhKpFIlaPlOOPUsNlt7Q3Qf8-GjQBx4WCN5HmemdGL0EtG3zLO2DtKORdSW8u05pLRR2jEacWJZtI8RqNDm_R9cYKelfKFUqqVUk_RCaPCSM7sCG2Wt4DnbbMltS9darb4IkYIHW4jXt4QZu0Ye3zdfoMaz87GH8_IZLnwBfBVc5vWqWvzGLcNnvZyTgFPQtrgzxAydKn_Tg1-327Lc_Qk-rrAi2M9RTeXF8vzGZl_ml6dT-YkVJIqwo2kTHNNqQFj_FrYymraP2a4COuojJYAkQG3VhnGjNExahE2EgywSolT9GaYe5fb-z2Uzu1SCVDXvoF2X5yyplKVMD1IBzDktpQM0d3ltPP5wTHqDsm6f5PtlVfH2fv1DjZ_CUOUPfD6CPgSfB2zb0IqfzhtjRCHG-WAfU81PPx3r_uwmC3kL48MXiod_Pjt-fzVKS20dKvrqZtLulpd6qmrxE92wZjj</recordid><startdate>199904</startdate><enddate>199904</enddate><creator>UCHIYAMA, KAZUYUKI</creator><creator>WAKATSUKI, DAISUKE</creator><creator>KAKINOKI, BUNPEI</creator><creator>TAKEUCHI, YOSHISHIGE</creator><creator>ARAKI, TSUTOMU</creator><creator>MORINAKA, YASUHIRO</creator><general>Blackwell Publishing Ltd</general><general>Pharmaceutical Press</general><scope>BSCLL</scope><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>199904</creationdate><title>The Long-lasting Effect of TU-199, a Novel H+,K+-ATPase Inhibitor, on Gastric Acid Secretion in Dogs</title><author>UCHIYAMA, KAZUYUKI ; WAKATSUKI, DAISUKE ; KAKINOKI, BUNPEI ; TAKEUCHI, YOSHISHIGE ; ARAKI, TSUTOMU ; MORINAKA, YASUHIRO</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4506-28501727008e88ab3949704971823cbf6875eef1e2996811887ff73cd5e8e1463</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><topic>2-Pyridinylmethylsulfinylbenzimidazoles</topic><topic>Analgesics, Non-Narcotic - pharmacology</topic><topic>Animals</topic><topic>Anti-Ulcer Agents - pharmacology</topic><topic>Biological and medical sciences</topic><topic>Carbachol - pharmacology</topic><topic>Digestive system</topic><topic>Dogs</topic><topic>Dose-Response Relationship, Drug</topic><topic>Enzyme Inhibitors - pharmacology</topic><topic>Female</topic><topic>Gastric Acid - metabolism</topic><topic>Gastric Fistula</topic><topic>Gastric Mucosa - drug effects</topic><topic>Gastric Mucosa - enzymology</topic><topic>Gastric Mucosa - metabolism</topic><topic>H(+)-K(+)-Exchanging ATPase - metabolism</topic><topic>Histamine - pharmacology</topic><topic>Hydrogen-Ion Concentration</topic><topic>Imidazoles - pharmacology</topic><topic>Lansoprazole</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Microsomes - drug effects</topic><topic>Microsomes - enzymology</topic><topic>Omeprazole - analogs & derivatives</topic><topic>Omeprazole - pharmacology</topic><topic>Pharmacology. Drug treatments</topic><topic>Proton Pump Inhibitors</topic><topic>Pyridines - pharmacology</topic><topic>Stomach - drug effects</topic><topic>Stomach - surgery</topic><topic>Tetragastrin - pharmacology</topic><topic>Time Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>UCHIYAMA, KAZUYUKI</creatorcontrib><creatorcontrib>WAKATSUKI, DAISUKE</creatorcontrib><creatorcontrib>KAKINOKI, BUNPEI</creatorcontrib><creatorcontrib>TAKEUCHI, YOSHISHIGE</creatorcontrib><creatorcontrib>ARAKI, TSUTOMU</creatorcontrib><creatorcontrib>MORINAKA, YASUHIRO</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of pharmacy and pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>UCHIYAMA, KAZUYUKI</au><au>WAKATSUKI, DAISUKE</au><au>KAKINOKI, BUNPEI</au><au>TAKEUCHI, YOSHISHIGE</au><au>ARAKI, TSUTOMU</au><au>MORINAKA, YASUHIRO</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The Long-lasting Effect of TU-199, a Novel H+,K+-ATPase Inhibitor, on Gastric Acid Secretion in Dogs</atitle><jtitle>Journal of pharmacy and pharmacology</jtitle><addtitle>J Pharm Pharmacol</addtitle><date>1999-04</date><risdate>1999</risdate><volume>51</volume><issue>4</issue><spage>457</spage><epage>464</epage><pages>457-464</pages><issn>0022-3573</issn><eissn>2042-7158</eissn><coden>JPPMAB</coden><abstract>We have used Heidenhain‐pouch dogs to investigate the effects of (±)‐5‐methoxy‐2‐{[(4‐methoxy‐3,5‐dimethylpyrid‐2‐yl)methyl]sulphinyl}‐1H‐imidazo[4,5‐b]pyridine (TU‐199), an imidazopyridine derivative, on gastric acid secretion stimulated by histamine, carbachol and tetragastrin. We have also investigated the duration of the antisecretory effect of TU‐199 using a measurement of intragastric pH for 24 h in gastric fistula dogs whose gastric acid secretion was stimulated by histamine.
Single oral administration of TU‐199 (0.1, 0.2 and 0.4 mg kg−1) dose‐dependently suppressed gastric acid secretion stimulated by histamine infusion. Oral treatment with TU‐199 (0.2, 0.4 and 0.8 mg kg−1) also dose‐dependently inhibited acid secretion induced by carbachol and tetragastrin. The inhibitory effect of TU‐199 on stimulated gastric acid secretion was more potent than that of omeprazole, a well‐known H+,K+‐ATPase inhibitor in dogs. Repeated oral treatment with TU‐199 at a dose of 0.2 mg kg−1 once a day for seven days markedly suppressed histamine‐stimulated gastric acid secretion in dogs. This inhibitory effect of TU‐199 reached a maximum level after three or four doses and was more pronounced than that of omeprazole or lansoprazole. In gastric fistula dogs, the duration of intragastric pH‐elevation by administration of TU‐199 (0.3 mg kg−1) was much longer than that of omeprazole (0.6 mg kg−1) or lansoprazole (0.9 mg kg−1). The IC50 values (doses resulting in 50% inhibition) of TU‐199, omeprazole and lansoprazole with regard to H+,K+‐ATPase activity in dog gastric mucosal microsomes were 8.6, 8.8 and 9.9 μM, respectively.
These results indicate that TU‐199 inhibits gastric acid secretion via suppression of a H+,K+‐ATPase activity. Our findings also suggest that TU‐199 might have potent and long‐lasting effects on gastric acid secretion.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>10385219</pmid><doi>10.1211/0022357991772510</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Journal of pharmacy and pharmacology, 1999-04, Vol.51 (4), p.457-464 |
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| subjects | 2-Pyridinylmethylsulfinylbenzimidazoles Analgesics, Non-Narcotic - pharmacology Animals Anti-Ulcer Agents - pharmacology Biological and medical sciences Carbachol - pharmacology Digestive system Dogs Dose-Response Relationship, Drug Enzyme Inhibitors - pharmacology Female Gastric Acid - metabolism Gastric Fistula Gastric Mucosa - drug effects Gastric Mucosa - enzymology Gastric Mucosa - metabolism H(+)-K(+)-Exchanging ATPase - metabolism Histamine - pharmacology Hydrogen-Ion Concentration Imidazoles - pharmacology Lansoprazole Male Medical sciences Microsomes - drug effects Microsomes - enzymology Omeprazole - analogs & derivatives Omeprazole - pharmacology Pharmacology. Drug treatments Proton Pump Inhibitors Pyridines - pharmacology Stomach - drug effects Stomach - surgery Tetragastrin - pharmacology Time Factors |
| title | The Long-lasting Effect of TU-199, a Novel H+,K+-ATPase Inhibitor, on Gastric Acid Secretion in Dogs |
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