Endothelium-dependent blunted membrane potential responses to ATP-sensitive K + channel modulators in aortae from rats with cirrhosis
Background/Aims: In vivo studies have shown that arterial vasodilation induced by synthetic openers of ATP-sensitive K + (K ATP) channels is decreased in rats with cirrhosis. Since vasodilation induced by these substances is mediated by membrane potential hyperpolarization in arterial smooth muscle...
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| Veröffentlicht in: | Journal of hepatology 1999, Vol.30 (1), p.107-114 |
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| creator | Lahaye, Philippe Fouassier, Laura Tazi, Khalid A Gottardi, Andrea De Fléjou, Jean-François Chagneau, Carine Rona, Jean-Pierre Housset, Chantal Reichen, Jürg Lebrec, Didier Moreau, Richard |
| description | Background/Aims: In vivo studies have shown that arterial vasodilation induced by synthetic openers of ATP-sensitive K
+ (K
ATP) channels is decreased in rats with cirrhosis. Since vasodilation induced by these substances is mediated by membrane potential hyperpolarization in arterial smooth muscle cells, membrane potential hyperpolarization in response to K
ATP channel openers may be altered in cirrhotic smooth muscle cells. The aim of the present study was to investigate the effects of K
ATP channel modulators (i.e. openers and blockers of these channels) on the membrane potential in smooth muscle cells in isolated aortae from cirrhotic and normal rats. The influence of endothelin-1 production by endothelial cells on smooth muscle cells membrane potential responses to K
ATP channel modulators was also studied.
Methods: Cells were impaled
in situ (in intact and endothelium-denuded aortae) with a microelectrode that was used to measure membrane potentials. K
ATP channel openers were diazoxide or cromakalim; blockers were glibenclamide or tolbutamide. Bosentan (a mixed endothelin receptor antagonist) and exogenous endothelin-1 were also used. Preproendothelin-1 mRNA was assayed in aortae by RNase protection assay. Aortic wall endothelin-1 concentration was measured by double antibody radioimmunoassay technique.
Results: As expected, in smooth muscle cells in intact normal aortae, K
ATP channel openers induced membrane potential hyperpolarization and K
ATP channel blockers membrane potential depolarization. In smooth muscle cells in intact cirrhotic aortae, K
ATP channel openers and blockers did not significantly change the membrane potential. Endothelium removal or exposure of intact aortae to bosentan restored normal membrane potential responses to K
ATP channel modulators in cirrhotic smooth muscle cells and did not alter the effects of these substances in normal smooth muscle cells. In endothelium-denuded aortae, exposure to exogenous endothelin-1 suppressed membrane potential responses to K
ATP channel modulators. In intact aortae, the abundance of preproendothelin-1 mRNA and endothelin-1 did not significantly differ between normal and cirrhotic rats.
Conclusions: K
ATP channel opener-induced membrane hyperpolarization and K
ATP channel blocker-elicited membrane depolarization are blunted in smooth muscle cells in intact cirrhotic aortae. This blunting is due to the activation of the endothelin-1 pathway in the aortic wall, downstream to the endothelial |
| doi_str_mv | 10.1016/S0168-8278(99)80014-2 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_69571783</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S0168827899800142</els_id><sourcerecordid>69571783</sourcerecordid><originalsourceid>FETCH-LOGICAL-c389t-cafdf7421424308ad439aac81e69e8f1cb259e251de0296419e7ce8a81d8bcd73</originalsourceid><addsrcrecordid>eNqFkNtqFTEUQIMo9Vj9hEIeRBQZTTK35ElKqRcsKFifQybZw4lkkjE7U_ED_G_TnkN99CUbste-LULOOHvDGR_efquPbKQY5UulXknGeNeIB2THB8YaNnT8IdndI4_JE8QfjLGWqe6EnCglRt6PO_LnMrpU9hD8tjQOVogOYqFT2GIBRxdYpmwi0DWV-u9NoBlwTREBaUn0_PprgxDRF38D9DN9Te3exAiBLsltwZSUkfpITcrFAJ1zWmg2BekvX_bU-pz3CT0-JY9mExCeHeMp-f7-8vriY3P15cOni_OrxrZSlcaa2c1jJ3gnupZJ47pWGWMlh0GBnLmdRK9A9NwBE6oqUDBakEZyJyfrxvaUvDj0XXP6uQEWvXi0EEI9MW2oB9WPfJRtBfsDaHNCzDDrNfvF5N-aM32rX9_p17dutVL6Tr8Wte7sOGCbFnD3VUffNf_8mDdoTZirW-vxX_O6s2B9xd4dMKgybjxkjdZDtOB8Blu0S_4_i_wFrKekYw</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>69571783</pqid></control><display><type>article</type><title>Endothelium-dependent blunted membrane potential responses to ATP-sensitive K + channel modulators in aortae from rats with cirrhosis</title><source>MEDLINE</source><source>Elsevier ScienceDirect Journals</source><creator>Lahaye, Philippe ; Fouassier, Laura ; Tazi, Khalid A ; Gottardi, Andrea De ; Fléjou, Jean-François ; Chagneau, Carine ; Rona, Jean-Pierre ; Housset, Chantal ; Reichen, Jürg ; Lebrec, Didier ; Moreau, Richard</creator><creatorcontrib>Lahaye, Philippe ; Fouassier, Laura ; Tazi, Khalid A ; Gottardi, Andrea De ; Fléjou, Jean-François ; Chagneau, Carine ; Rona, Jean-Pierre ; Housset, Chantal ; Reichen, Jürg ; Lebrec, Didier ; Moreau, Richard</creatorcontrib><description>Background/Aims: In vivo studies have shown that arterial vasodilation induced by synthetic openers of ATP-sensitive K
+ (K
ATP) channels is decreased in rats with cirrhosis. Since vasodilation induced by these substances is mediated by membrane potential hyperpolarization in arterial smooth muscle cells, membrane potential hyperpolarization in response to K
ATP channel openers may be altered in cirrhotic smooth muscle cells. The aim of the present study was to investigate the effects of K
ATP channel modulators (i.e. openers and blockers of these channels) on the membrane potential in smooth muscle cells in isolated aortae from cirrhotic and normal rats. The influence of endothelin-1 production by endothelial cells on smooth muscle cells membrane potential responses to K
ATP channel modulators was also studied.
Methods: Cells were impaled
in situ (in intact and endothelium-denuded aortae) with a microelectrode that was used to measure membrane potentials. K
ATP channel openers were diazoxide or cromakalim; blockers were glibenclamide or tolbutamide. Bosentan (a mixed endothelin receptor antagonist) and exogenous endothelin-1 were also used. Preproendothelin-1 mRNA was assayed in aortae by RNase protection assay. Aortic wall endothelin-1 concentration was measured by double antibody radioimmunoassay technique.
Results: As expected, in smooth muscle cells in intact normal aortae, K
ATP channel openers induced membrane potential hyperpolarization and K
ATP channel blockers membrane potential depolarization. In smooth muscle cells in intact cirrhotic aortae, K
ATP channel openers and blockers did not significantly change the membrane potential. Endothelium removal or exposure of intact aortae to bosentan restored normal membrane potential responses to K
ATP channel modulators in cirrhotic smooth muscle cells and did not alter the effects of these substances in normal smooth muscle cells. In endothelium-denuded aortae, exposure to exogenous endothelin-1 suppressed membrane potential responses to K
ATP channel modulators. In intact aortae, the abundance of preproendothelin-1 mRNA and endothelin-1 did not significantly differ between normal and cirrhotic rats.
Conclusions: K
ATP channel opener-induced membrane hyperpolarization and K
ATP channel blocker-elicited membrane depolarization are blunted in smooth muscle cells in intact cirrhotic aortae. This blunting is due to the activation of the endothelin-1 pathway in the aortic wall, downstream to the endothelial production of endothelin-1.</description><identifier>ISSN: 0168-8278</identifier><identifier>EISSN: 1600-0641</identifier><identifier>DOI: 10.1016/S0168-8278(99)80014-2</identifier><identifier>PMID: 9927157</identifier><identifier>CODEN: JOHEEC</identifier><language>eng</language><publisher>Oxford: Elsevier B.V</publisher><subject>Adenosine Triphosphate - physiology ; Animals ; Aorta - metabolism ; Aorta - physiopathology ; Biological and medical sciences ; Bosentan ; Cromakalim - pharmacology ; Diazoxide - pharmacology ; Endothelin-1 ; Endothelin-1 - pharmacology ; Endothelium, Vascular - physiopathology ; Gastroenterology. Liver. Pancreas. Abdomen ; Glyburide - pharmacology ; K ATP channel blockers ; K ATP channel openers ; Liver Cirrhosis, Experimental - physiopathology ; Liver. Biliary tract. Portal circulation. Exocrine pancreas ; Male ; Medical sciences ; Membrane potential depolarization ; Membrane potential hyperpolarization ; Membrane Potentials - drug effects ; Membrane Potentials - physiology ; Other diseases. Semiology ; Portal hypertension ; Potassium Channel Blockers ; Potassium Channels - drug effects ; Potassium Channels - physiology ; Rats ; Rats, Sprague-Dawley ; Sulfonamides - pharmacology ; Tolbutamide - pharmacology</subject><ispartof>Journal of hepatology, 1999, Vol.30 (1), p.107-114</ispartof><rights>1999</rights><rights>1999 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c389t-cafdf7421424308ad439aac81e69e8f1cb259e251de0296419e7ce8a81d8bcd73</citedby><cites>FETCH-LOGICAL-c389t-cafdf7421424308ad439aac81e69e8f1cb259e251de0296419e7ce8a81d8bcd73</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0168827899800142$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,4010,27900,27901,27902,65306</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1641205$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9927157$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lahaye, Philippe</creatorcontrib><creatorcontrib>Fouassier, Laura</creatorcontrib><creatorcontrib>Tazi, Khalid A</creatorcontrib><creatorcontrib>Gottardi, Andrea De</creatorcontrib><creatorcontrib>Fléjou, Jean-François</creatorcontrib><creatorcontrib>Chagneau, Carine</creatorcontrib><creatorcontrib>Rona, Jean-Pierre</creatorcontrib><creatorcontrib>Housset, Chantal</creatorcontrib><creatorcontrib>Reichen, Jürg</creatorcontrib><creatorcontrib>Lebrec, Didier</creatorcontrib><creatorcontrib>Moreau, Richard</creatorcontrib><title>Endothelium-dependent blunted membrane potential responses to ATP-sensitive K + channel modulators in aortae from rats with cirrhosis</title><title>Journal of hepatology</title><addtitle>J Hepatol</addtitle><description>Background/Aims: In vivo studies have shown that arterial vasodilation induced by synthetic openers of ATP-sensitive K
+ (K
ATP) channels is decreased in rats with cirrhosis. Since vasodilation induced by these substances is mediated by membrane potential hyperpolarization in arterial smooth muscle cells, membrane potential hyperpolarization in response to K
ATP channel openers may be altered in cirrhotic smooth muscle cells. The aim of the present study was to investigate the effects of K
ATP channel modulators (i.e. openers and blockers of these channels) on the membrane potential in smooth muscle cells in isolated aortae from cirrhotic and normal rats. The influence of endothelin-1 production by endothelial cells on smooth muscle cells membrane potential responses to K
ATP channel modulators was also studied.
Methods: Cells were impaled
in situ (in intact and endothelium-denuded aortae) with a microelectrode that was used to measure membrane potentials. K
ATP channel openers were diazoxide or cromakalim; blockers were glibenclamide or tolbutamide. Bosentan (a mixed endothelin receptor antagonist) and exogenous endothelin-1 were also used. Preproendothelin-1 mRNA was assayed in aortae by RNase protection assay. Aortic wall endothelin-1 concentration was measured by double antibody radioimmunoassay technique.
Results: As expected, in smooth muscle cells in intact normal aortae, K
ATP channel openers induced membrane potential hyperpolarization and K
ATP channel blockers membrane potential depolarization. In smooth muscle cells in intact cirrhotic aortae, K
ATP channel openers and blockers did not significantly change the membrane potential. Endothelium removal or exposure of intact aortae to bosentan restored normal membrane potential responses to K
ATP channel modulators in cirrhotic smooth muscle cells and did not alter the effects of these substances in normal smooth muscle cells. In endothelium-denuded aortae, exposure to exogenous endothelin-1 suppressed membrane potential responses to K
ATP channel modulators. In intact aortae, the abundance of preproendothelin-1 mRNA and endothelin-1 did not significantly differ between normal and cirrhotic rats.
Conclusions: K
ATP channel opener-induced membrane hyperpolarization and K
ATP channel blocker-elicited membrane depolarization are blunted in smooth muscle cells in intact cirrhotic aortae. This blunting is due to the activation of the endothelin-1 pathway in the aortic wall, downstream to the endothelial production of endothelin-1.</description><subject>Adenosine Triphosphate - physiology</subject><subject>Animals</subject><subject>Aorta - metabolism</subject><subject>Aorta - physiopathology</subject><subject>Biological and medical sciences</subject><subject>Bosentan</subject><subject>Cromakalim - pharmacology</subject><subject>Diazoxide - pharmacology</subject><subject>Endothelin-1</subject><subject>Endothelin-1 - pharmacology</subject><subject>Endothelium, Vascular - physiopathology</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Glyburide - pharmacology</subject><subject>K ATP channel blockers</subject><subject>K ATP channel openers</subject><subject>Liver Cirrhosis, Experimental - physiopathology</subject><subject>Liver. Biliary tract. Portal circulation. Exocrine pancreas</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Membrane potential depolarization</subject><subject>Membrane potential hyperpolarization</subject><subject>Membrane Potentials - drug effects</subject><subject>Membrane Potentials - physiology</subject><subject>Other diseases. Semiology</subject><subject>Portal hypertension</subject><subject>Potassium Channel Blockers</subject><subject>Potassium Channels - drug effects</subject><subject>Potassium Channels - physiology</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Sulfonamides - pharmacology</subject><subject>Tolbutamide - pharmacology</subject><issn>0168-8278</issn><issn>1600-0641</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkNtqFTEUQIMo9Vj9hEIeRBQZTTK35ElKqRcsKFifQybZw4lkkjE7U_ED_G_TnkN99CUbste-LULOOHvDGR_efquPbKQY5UulXknGeNeIB2THB8YaNnT8IdndI4_JE8QfjLGWqe6EnCglRt6PO_LnMrpU9hD8tjQOVogOYqFT2GIBRxdYpmwi0DWV-u9NoBlwTREBaUn0_PprgxDRF38D9DN9Te3exAiBLsltwZSUkfpITcrFAJ1zWmg2BekvX_bU-pz3CT0-JY9mExCeHeMp-f7-8vriY3P15cOni_OrxrZSlcaa2c1jJ3gnupZJ47pWGWMlh0GBnLmdRK9A9NwBE6oqUDBakEZyJyfrxvaUvDj0XXP6uQEWvXi0EEI9MW2oB9WPfJRtBfsDaHNCzDDrNfvF5N-aM32rX9_p17dutVL6Tr8Wte7sOGCbFnD3VUffNf_8mDdoTZirW-vxX_O6s2B9xd4dMKgybjxkjdZDtOB8Blu0S_4_i_wFrKekYw</recordid><startdate>1999</startdate><enddate>1999</enddate><creator>Lahaye, Philippe</creator><creator>Fouassier, Laura</creator><creator>Tazi, Khalid A</creator><creator>Gottardi, Andrea De</creator><creator>Fléjou, Jean-François</creator><creator>Chagneau, Carine</creator><creator>Rona, Jean-Pierre</creator><creator>Housset, Chantal</creator><creator>Reichen, Jürg</creator><creator>Lebrec, Didier</creator><creator>Moreau, Richard</creator><general>Elsevier B.V</general><general>Elsevier</general><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>1999</creationdate><title>Endothelium-dependent blunted membrane potential responses to ATP-sensitive K + channel modulators in aortae from rats with cirrhosis</title><author>Lahaye, Philippe ; Fouassier, Laura ; Tazi, Khalid A ; Gottardi, Andrea De ; Fléjou, Jean-François ; Chagneau, Carine ; Rona, Jean-Pierre ; Housset, Chantal ; Reichen, Jürg ; Lebrec, Didier ; Moreau, Richard</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c389t-cafdf7421424308ad439aac81e69e8f1cb259e251de0296419e7ce8a81d8bcd73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><topic>Adenosine Triphosphate - physiology</topic><topic>Animals</topic><topic>Aorta - metabolism</topic><topic>Aorta - physiopathology</topic><topic>Biological and medical sciences</topic><topic>Bosentan</topic><topic>Cromakalim - pharmacology</topic><topic>Diazoxide - pharmacology</topic><topic>Endothelin-1</topic><topic>Endothelin-1 - pharmacology</topic><topic>Endothelium, Vascular - physiopathology</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>Glyburide - pharmacology</topic><topic>K ATP channel blockers</topic><topic>K ATP channel openers</topic><topic>Liver Cirrhosis, Experimental - physiopathology</topic><topic>Liver. Biliary tract. Portal circulation. Exocrine pancreas</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Membrane potential depolarization</topic><topic>Membrane potential hyperpolarization</topic><topic>Membrane Potentials - drug effects</topic><topic>Membrane Potentials - physiology</topic><topic>Other diseases. Semiology</topic><topic>Portal hypertension</topic><topic>Potassium Channel Blockers</topic><topic>Potassium Channels - drug effects</topic><topic>Potassium Channels - physiology</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Sulfonamides - pharmacology</topic><topic>Tolbutamide - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lahaye, Philippe</creatorcontrib><creatorcontrib>Fouassier, Laura</creatorcontrib><creatorcontrib>Tazi, Khalid A</creatorcontrib><creatorcontrib>Gottardi, Andrea De</creatorcontrib><creatorcontrib>Fléjou, Jean-François</creatorcontrib><creatorcontrib>Chagneau, Carine</creatorcontrib><creatorcontrib>Rona, Jean-Pierre</creatorcontrib><creatorcontrib>Housset, Chantal</creatorcontrib><creatorcontrib>Reichen, Jürg</creatorcontrib><creatorcontrib>Lebrec, Didier</creatorcontrib><creatorcontrib>Moreau, Richard</creatorcontrib><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 hepatology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lahaye, Philippe</au><au>Fouassier, Laura</au><au>Tazi, Khalid A</au><au>Gottardi, Andrea De</au><au>Fléjou, Jean-François</au><au>Chagneau, Carine</au><au>Rona, Jean-Pierre</au><au>Housset, Chantal</au><au>Reichen, Jürg</au><au>Lebrec, Didier</au><au>Moreau, Richard</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Endothelium-dependent blunted membrane potential responses to ATP-sensitive K + channel modulators in aortae from rats with cirrhosis</atitle><jtitle>Journal of hepatology</jtitle><addtitle>J Hepatol</addtitle><date>1999</date><risdate>1999</risdate><volume>30</volume><issue>1</issue><spage>107</spage><epage>114</epage><pages>107-114</pages><issn>0168-8278</issn><eissn>1600-0641</eissn><coden>JOHEEC</coden><abstract>Background/Aims: In vivo studies have shown that arterial vasodilation induced by synthetic openers of ATP-sensitive K
+ (K
ATP) channels is decreased in rats with cirrhosis. Since vasodilation induced by these substances is mediated by membrane potential hyperpolarization in arterial smooth muscle cells, membrane potential hyperpolarization in response to K
ATP channel openers may be altered in cirrhotic smooth muscle cells. The aim of the present study was to investigate the effects of K
ATP channel modulators (i.e. openers and blockers of these channels) on the membrane potential in smooth muscle cells in isolated aortae from cirrhotic and normal rats. The influence of endothelin-1 production by endothelial cells on smooth muscle cells membrane potential responses to K
ATP channel modulators was also studied.
Methods: Cells were impaled
in situ (in intact and endothelium-denuded aortae) with a microelectrode that was used to measure membrane potentials. K
ATP channel openers were diazoxide or cromakalim; blockers were glibenclamide or tolbutamide. Bosentan (a mixed endothelin receptor antagonist) and exogenous endothelin-1 were also used. Preproendothelin-1 mRNA was assayed in aortae by RNase protection assay. Aortic wall endothelin-1 concentration was measured by double antibody radioimmunoassay technique.
Results: As expected, in smooth muscle cells in intact normal aortae, K
ATP channel openers induced membrane potential hyperpolarization and K
ATP channel blockers membrane potential depolarization. In smooth muscle cells in intact cirrhotic aortae, K
ATP channel openers and blockers did not significantly change the membrane potential. Endothelium removal or exposure of intact aortae to bosentan restored normal membrane potential responses to K
ATP channel modulators in cirrhotic smooth muscle cells and did not alter the effects of these substances in normal smooth muscle cells. In endothelium-denuded aortae, exposure to exogenous endothelin-1 suppressed membrane potential responses to K
ATP channel modulators. In intact aortae, the abundance of preproendothelin-1 mRNA and endothelin-1 did not significantly differ between normal and cirrhotic rats.
Conclusions: K
ATP channel opener-induced membrane hyperpolarization and K
ATP channel blocker-elicited membrane depolarization are blunted in smooth muscle cells in intact cirrhotic aortae. This blunting is due to the activation of the endothelin-1 pathway in the aortic wall, downstream to the endothelial production of endothelin-1.</abstract><cop>Oxford</cop><pub>Elsevier B.V</pub><pmid>9927157</pmid><doi>10.1016/S0168-8278(99)80014-2</doi><tpages>8</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0168-8278 |
| ispartof | Journal of hepatology, 1999, Vol.30 (1), p.107-114 |
| issn | 0168-8278 1600-0641 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_69571783 |
| source | MEDLINE; Elsevier ScienceDirect Journals |
| subjects | Adenosine Triphosphate - physiology Animals Aorta - metabolism Aorta - physiopathology Biological and medical sciences Bosentan Cromakalim - pharmacology Diazoxide - pharmacology Endothelin-1 Endothelin-1 - pharmacology Endothelium, Vascular - physiopathology Gastroenterology. Liver. Pancreas. Abdomen Glyburide - pharmacology K ATP channel blockers K ATP channel openers Liver Cirrhosis, Experimental - physiopathology Liver. Biliary tract. Portal circulation. Exocrine pancreas Male Medical sciences Membrane potential depolarization Membrane potential hyperpolarization Membrane Potentials - drug effects Membrane Potentials - physiology Other diseases. Semiology Portal hypertension Potassium Channel Blockers Potassium Channels - drug effects Potassium Channels - physiology Rats Rats, Sprague-Dawley Sulfonamides - pharmacology Tolbutamide - pharmacology |
| title | Endothelium-dependent blunted membrane potential responses to ATP-sensitive K + channel modulators in aortae from rats with cirrhosis |
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