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K+ channel modulation of slow wave activity in the guinea‐pig prostate
Background and purpose: The aim of this study was to investigate the role of different K+ channel populations and the inhibitory effect of various exogenously applied K+ channel openers in the regulation of slow wave activity in the guinea‐pig prostate. Experimental approach: Recordings of membrane...
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| Published in: | British journal of pharmacology 2007-07, Vol.151 (6), p.828-836 |
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| container_title | British journal of pharmacology |
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| creator | Nguyen, D‐T T Lang, R J Exintaris, B |
| description | Background and purpose:
The aim of this study was to investigate the role of different K+ channel populations and the inhibitory effect of various exogenously applied K+ channel openers in the regulation of slow wave activity in the guinea‐pig prostate.
Experimental approach:
Recordings of membrane potential were made using intracellular microelectrodes.
Key results:
Tetraethylammonium (TEA 300 μM and 1 mM), iberiotoxin (150 nM) and 4‐aminopyridine (4‐AP 1 mM) increased the frequency of slow wave discharge. Apamin (1–200 nM) and glibenclamide (1 μM) had no effect on slow wave activity. Lemakalim (1 μM) and PCO‐400 (1 μM) abolished the slow waves, as did sodium nitroprusside (SNP 10 μM) and calcitonin gene‐related peptide (CGRP 100 nM). The inhibitory effect of these agents was independent of a significant change in membrane potential. In the presence of 4‐AP (1 mM), TEA (1 mM) or glibenclamide (1 μM) the inhibitory actions of SNP (10 μM) were attenuated. The inhibitory actions of CGRP (100 nM) were also reversed by glibenclamide (1 μM). In contrast, isoprenaline (1 μM) did not alter the frequency of slow wave discharge.
Conclusions and implications:
These results demonstrate that BKCa and 4‐AP‐sensitive K+ channels regulate the frequency of prostatic slow wave discharge. SNP and CGRP abolish slow waves in a hyperpolarisation‐independent manner, partially via opening of KATP channels. BKCa and 4‐AP‐sensitive K+ channels also play an important role in the SNP‐induced inhibition of slow wave activity. The lack of membrane hyperpolarisation associated with the SNP‐ and CGRP‐induced inhibition implies that the channels involved in this action are not predominantly located on the smooth muscle cells.
British Journal of Pharmacology (2007) 151, 828–836; doi:10.1038/sj.bjp.0707283 |
| doi_str_mv | 10.1038/sj.bjp.0707283 |
| format | article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_2014131</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>70719892</sourcerecordid><originalsourceid>FETCH-LOGICAL-c5547-52bf5703579f2e86a0f0139659f221bbc812b55dbe6945c0c62d36bb2aa821d3</originalsourceid><addsrcrecordid>eNqFkc1u1DAUha2qqB0K2y6RVQk2KIN_4tjZIEEFDGqlsujesh1nxpHHDnEyo9nxCDwjT4KriWhhw-rKup_PPfceAC4xWmJExbvULXXXLxFHnAh6Aha45FXBqMCnYIEQ4gXGQpyD5yl1COUmZ2fgHHNGaUnYAqxu3kKzUSFYD7exmbwaXQwwtjD5uId7tbNQmdHt3HiALsBxY-F6csGqXz9-9m4N-yGmUY32BXjWKp_sy7legPvPn-6vV8Xt3Zev1x9uC8NYyQtGdMs4oozXLbGiUqhFmNYVy0-CtTYCE81Yo21Vl8wgU5GGVloTpQTBDb0A74-y_aS3tjE2jIPysh_cVg0HGZWTf3eC28h13EmSl8cUZ4E3s8AQv082jXLrkrHeq2DjlGQ-JK5FTTJ49Q_YxWkIeTdJcGbKunqAlkfI5DOkwbZ_nGAkHwKSqZM5IDkHlD-8eur_EZ8TycDrGVDJKN8OKhiXHrlsjXCKMkeO3N55e_jPWPnx26qsOP0Nku-qdA</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>217194962</pqid></control><display><type>article</type><title>K+ channel modulation of slow wave activity in the guinea‐pig prostate</title><source>Wiley-Blackwell Read & Publish Collection</source><source>PubMed Central</source><creator>Nguyen, D‐T T ; Lang, R J ; Exintaris, B</creator><creatorcontrib>Nguyen, D‐T T ; Lang, R J ; Exintaris, B</creatorcontrib><description>Background and purpose:
The aim of this study was to investigate the role of different K+ channel populations and the inhibitory effect of various exogenously applied K+ channel openers in the regulation of slow wave activity in the guinea‐pig prostate.
Experimental approach:
Recordings of membrane potential were made using intracellular microelectrodes.
Key results:
Tetraethylammonium (TEA 300 μM and 1 mM), iberiotoxin (150 nM) and 4‐aminopyridine (4‐AP 1 mM) increased the frequency of slow wave discharge. Apamin (1–200 nM) and glibenclamide (1 μM) had no effect on slow wave activity. Lemakalim (1 μM) and PCO‐400 (1 μM) abolished the slow waves, as did sodium nitroprusside (SNP 10 μM) and calcitonin gene‐related peptide (CGRP 100 nM). The inhibitory effect of these agents was independent of a significant change in membrane potential. In the presence of 4‐AP (1 mM), TEA (1 mM) or glibenclamide (1 μM) the inhibitory actions of SNP (10 μM) were attenuated. The inhibitory actions of CGRP (100 nM) were also reversed by glibenclamide (1 μM). In contrast, isoprenaline (1 μM) did not alter the frequency of slow wave discharge.
Conclusions and implications:
These results demonstrate that BKCa and 4‐AP‐sensitive K+ channels regulate the frequency of prostatic slow wave discharge. SNP and CGRP abolish slow waves in a hyperpolarisation‐independent manner, partially via opening of KATP channels. BKCa and 4‐AP‐sensitive K+ channels also play an important role in the SNP‐induced inhibition of slow wave activity. The lack of membrane hyperpolarisation associated with the SNP‐ and CGRP‐induced inhibition implies that the channels involved in this action are not predominantly located on the smooth muscle cells.
British Journal of Pharmacology (2007) 151, 828–836; doi:10.1038/sj.bjp.0707283</description><identifier>ISSN: 0007-1188</identifier><identifier>EISSN: 1476-5381</identifier><identifier>DOI: 10.1038/sj.bjp.0707283</identifier><identifier>PMID: 17533425</identifier><identifier>CODEN: BJPCBM</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>4-Aminopyridine - pharmacology ; Animals ; Apamin - administration & dosage ; Apamin - pharmacology ; Benzopyrans - pharmacology ; Biological and medical sciences ; Calcitonin Gene-Related Peptide - pharmacology ; Cromakalim - pharmacology ; Cyclopentanes - pharmacology ; Dose-Response Relationship, Drug ; Electrophysiology ; Glyburide - pharmacology ; Guinea Pigs ; In Vitro Techniques ; Isoproterenol - pharmacology ; K+ channel blockers ; Male ; Medical sciences ; Membrane Potentials ; Nitroprusside - pharmacology ; Peptides - pharmacology ; Pharmacology. Drug treatments ; Potassium Channel Blockers - pharmacology ; Potassium Channels - agonists ; Potassium Channels - physiology ; prostate ; Prostate - metabolism ; Prostate - physiology ; Research Papers ; slow waves ; smooth muscle ; Stromal Cells - drug effects ; Stromal Cells - metabolism ; Tetraethylammonium - administration & dosage ; Tetraethylammonium - pharmacology</subject><ispartof>British journal of pharmacology, 2007-07, Vol.151 (6), p.828-836</ispartof><rights>2007 British Pharmacological Society</rights><rights>2007 INIST-CNRS</rights><rights>Copyright Nature Publishing Group Jul 2007</rights><rights>Copyright 2007, Nature Publishing Group 2007 Nature Publishing Group</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5547-52bf5703579f2e86a0f0139659f221bbc812b55dbe6945c0c62d36bb2aa821d3</citedby><cites>FETCH-LOGICAL-c5547-52bf5703579f2e86a0f0139659f221bbc812b55dbe6945c0c62d36bb2aa821d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2014131/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2014131/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=18922730$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17533425$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Nguyen, D‐T T</creatorcontrib><creatorcontrib>Lang, R J</creatorcontrib><creatorcontrib>Exintaris, B</creatorcontrib><title>K+ channel modulation of slow wave activity in the guinea‐pig prostate</title><title>British journal of pharmacology</title><addtitle>Br J Pharmacol</addtitle><description>Background and purpose:
The aim of this study was to investigate the role of different K+ channel populations and the inhibitory effect of various exogenously applied K+ channel openers in the regulation of slow wave activity in the guinea‐pig prostate.
Experimental approach:
Recordings of membrane potential were made using intracellular microelectrodes.
Key results:
Tetraethylammonium (TEA 300 μM and 1 mM), iberiotoxin (150 nM) and 4‐aminopyridine (4‐AP 1 mM) increased the frequency of slow wave discharge. Apamin (1–200 nM) and glibenclamide (1 μM) had no effect on slow wave activity. Lemakalim (1 μM) and PCO‐400 (1 μM) abolished the slow waves, as did sodium nitroprusside (SNP 10 μM) and calcitonin gene‐related peptide (CGRP 100 nM). The inhibitory effect of these agents was independent of a significant change in membrane potential. In the presence of 4‐AP (1 mM), TEA (1 mM) or glibenclamide (1 μM) the inhibitory actions of SNP (10 μM) were attenuated. The inhibitory actions of CGRP (100 nM) were also reversed by glibenclamide (1 μM). In contrast, isoprenaline (1 μM) did not alter the frequency of slow wave discharge.
Conclusions and implications:
These results demonstrate that BKCa and 4‐AP‐sensitive K+ channels regulate the frequency of prostatic slow wave discharge. SNP and CGRP abolish slow waves in a hyperpolarisation‐independent manner, partially via opening of KATP channels. BKCa and 4‐AP‐sensitive K+ channels also play an important role in the SNP‐induced inhibition of slow wave activity. The lack of membrane hyperpolarisation associated with the SNP‐ and CGRP‐induced inhibition implies that the channels involved in this action are not predominantly located on the smooth muscle cells.
British Journal of Pharmacology (2007) 151, 828–836; doi:10.1038/sj.bjp.0707283</description><subject>4-Aminopyridine - pharmacology</subject><subject>Animals</subject><subject>Apamin - administration & dosage</subject><subject>Apamin - pharmacology</subject><subject>Benzopyrans - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Calcitonin Gene-Related Peptide - pharmacology</subject><subject>Cromakalim - pharmacology</subject><subject>Cyclopentanes - pharmacology</subject><subject>Dose-Response Relationship, Drug</subject><subject>Electrophysiology</subject><subject>Glyburide - pharmacology</subject><subject>Guinea Pigs</subject><subject>In Vitro Techniques</subject><subject>Isoproterenol - pharmacology</subject><subject>K+ channel blockers</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Membrane Potentials</subject><subject>Nitroprusside - pharmacology</subject><subject>Peptides - pharmacology</subject><subject>Pharmacology. Drug treatments</subject><subject>Potassium Channel Blockers - pharmacology</subject><subject>Potassium Channels - agonists</subject><subject>Potassium Channels - physiology</subject><subject>prostate</subject><subject>Prostate - metabolism</subject><subject>Prostate - physiology</subject><subject>Research Papers</subject><subject>slow waves</subject><subject>smooth muscle</subject><subject>Stromal Cells - drug effects</subject><subject>Stromal Cells - metabolism</subject><subject>Tetraethylammonium - administration & dosage</subject><subject>Tetraethylammonium - pharmacology</subject><issn>0007-1188</issn><issn>1476-5381</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><recordid>eNqFkc1u1DAUha2qqB0K2y6RVQk2KIN_4tjZIEEFDGqlsujesh1nxpHHDnEyo9nxCDwjT4KriWhhw-rKup_PPfceAC4xWmJExbvULXXXLxFHnAh6Aha45FXBqMCnYIEQ4gXGQpyD5yl1COUmZ2fgHHNGaUnYAqxu3kKzUSFYD7exmbwaXQwwtjD5uId7tbNQmdHt3HiALsBxY-F6csGqXz9-9m4N-yGmUY32BXjWKp_sy7legPvPn-6vV8Xt3Zev1x9uC8NYyQtGdMs4oozXLbGiUqhFmNYVy0-CtTYCE81Yo21Vl8wgU5GGVloTpQTBDb0A74-y_aS3tjE2jIPysh_cVg0HGZWTf3eC28h13EmSl8cUZ4E3s8AQv082jXLrkrHeq2DjlGQ-JK5FTTJ49Q_YxWkIeTdJcGbKunqAlkfI5DOkwbZ_nGAkHwKSqZM5IDkHlD-8eur_EZ8TycDrGVDJKN8OKhiXHrlsjXCKMkeO3N55e_jPWPnx26qsOP0Nku-qdA</recordid><startdate>200707</startdate><enddate>200707</enddate><creator>Nguyen, D‐T T</creator><creator>Lang, R J</creator><creator>Exintaris, B</creator><general>Blackwell Publishing Ltd</general><general>Nature Publishing</general><general>Nature Publishing Group</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>3V.</scope><scope>7QP</scope><scope>7RV</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>200707</creationdate><title>K+ channel modulation of slow wave activity in the guinea‐pig prostate</title><author>Nguyen, D‐T T ; Lang, R J ; Exintaris, B</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5547-52bf5703579f2e86a0f0139659f221bbc812b55dbe6945c0c62d36bb2aa821d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>4-Aminopyridine - pharmacology</topic><topic>Animals</topic><topic>Apamin - administration & dosage</topic><topic>Apamin - pharmacology</topic><topic>Benzopyrans - pharmacology</topic><topic>Biological and medical sciences</topic><topic>Calcitonin Gene-Related Peptide - pharmacology</topic><topic>Cromakalim - pharmacology</topic><topic>Cyclopentanes - pharmacology</topic><topic>Dose-Response Relationship, Drug</topic><topic>Electrophysiology</topic><topic>Glyburide - pharmacology</topic><topic>Guinea Pigs</topic><topic>In Vitro Techniques</topic><topic>Isoproterenol - pharmacology</topic><topic>K+ channel blockers</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Membrane Potentials</topic><topic>Nitroprusside - pharmacology</topic><topic>Peptides - pharmacology</topic><topic>Pharmacology. Drug treatments</topic><topic>Potassium Channel Blockers - pharmacology</topic><topic>Potassium Channels - agonists</topic><topic>Potassium Channels - physiology</topic><topic>prostate</topic><topic>Prostate - metabolism</topic><topic>Prostate - physiology</topic><topic>Research Papers</topic><topic>slow waves</topic><topic>smooth muscle</topic><topic>Stromal Cells - drug effects</topic><topic>Stromal Cells - metabolism</topic><topic>Tetraethylammonium - administration & dosage</topic><topic>Tetraethylammonium - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Nguyen, D‐T T</creatorcontrib><creatorcontrib>Lang, R J</creatorcontrib><creatorcontrib>Exintaris, B</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>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</collection><collection>Biological Science Database</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>British journal of pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Nguyen, D‐T T</au><au>Lang, R J</au><au>Exintaris, B</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>K+ channel modulation of slow wave activity in the guinea‐pig prostate</atitle><jtitle>British journal of pharmacology</jtitle><addtitle>Br J Pharmacol</addtitle><date>2007-07</date><risdate>2007</risdate><volume>151</volume><issue>6</issue><spage>828</spage><epage>836</epage><pages>828-836</pages><issn>0007-1188</issn><eissn>1476-5381</eissn><coden>BJPCBM</coden><abstract>Background and purpose:
The aim of this study was to investigate the role of different K+ channel populations and the inhibitory effect of various exogenously applied K+ channel openers in the regulation of slow wave activity in the guinea‐pig prostate.
Experimental approach:
Recordings of membrane potential were made using intracellular microelectrodes.
Key results:
Tetraethylammonium (TEA 300 μM and 1 mM), iberiotoxin (150 nM) and 4‐aminopyridine (4‐AP 1 mM) increased the frequency of slow wave discharge. Apamin (1–200 nM) and glibenclamide (1 μM) had no effect on slow wave activity. Lemakalim (1 μM) and PCO‐400 (1 μM) abolished the slow waves, as did sodium nitroprusside (SNP 10 μM) and calcitonin gene‐related peptide (CGRP 100 nM). The inhibitory effect of these agents was independent of a significant change in membrane potential. In the presence of 4‐AP (1 mM), TEA (1 mM) or glibenclamide (1 μM) the inhibitory actions of SNP (10 μM) were attenuated. The inhibitory actions of CGRP (100 nM) were also reversed by glibenclamide (1 μM). In contrast, isoprenaline (1 μM) did not alter the frequency of slow wave discharge.
Conclusions and implications:
These results demonstrate that BKCa and 4‐AP‐sensitive K+ channels regulate the frequency of prostatic slow wave discharge. SNP and CGRP abolish slow waves in a hyperpolarisation‐independent manner, partially via opening of KATP channels. BKCa and 4‐AP‐sensitive K+ channels also play an important role in the SNP‐induced inhibition of slow wave activity. The lack of membrane hyperpolarisation associated with the SNP‐ and CGRP‐induced inhibition implies that the channels involved in this action are not predominantly located on the smooth muscle cells.
British Journal of Pharmacology (2007) 151, 828–836; doi:10.1038/sj.bjp.0707283</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>17533425</pmid><doi>10.1038/sj.bjp.0707283</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | British journal of pharmacology, 2007-07, Vol.151 (6), p.828-836 |
| issn | 0007-1188 1476-5381 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_2014131 |
| source | Wiley-Blackwell Read & Publish Collection; PubMed Central |
| subjects | 4-Aminopyridine - pharmacology Animals Apamin - administration & dosage Apamin - pharmacology Benzopyrans - pharmacology Biological and medical sciences Calcitonin Gene-Related Peptide - pharmacology Cromakalim - pharmacology Cyclopentanes - pharmacology Dose-Response Relationship, Drug Electrophysiology Glyburide - pharmacology Guinea Pigs In Vitro Techniques Isoproterenol - pharmacology K+ channel blockers Male Medical sciences Membrane Potentials Nitroprusside - pharmacology Peptides - pharmacology Pharmacology. Drug treatments Potassium Channel Blockers - pharmacology Potassium Channels - agonists Potassium Channels - physiology prostate Prostate - metabolism Prostate - physiology Research Papers slow waves smooth muscle Stromal Cells - drug effects Stromal Cells - metabolism Tetraethylammonium - administration & dosage Tetraethylammonium - pharmacology |
| title | K+ channel modulation of slow wave activity in the guinea‐pig prostate |
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