Contribution of K+ channels to endothelium-derived hypolarization-induced renal vasodilation in rats in vivo and in vitro
We investigated the mechanisms behind the endothelial-derived hyperpolarization (EDH)-induced renal vasodilation in vivo and in vitro in rats. We assessed the role of Ca 2+ -activated K + channels and whether K + released from the endothelial cells activates inward rectifier K + (K ir ) channels and...
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| Veröffentlicht in: | Pflügers Archiv 2016-07, Vol.468 (7), p.1139-1149 |
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| creator | Rasmussen, Kasper Moller Boje Braunstein, Thomas Hartig Salomonsson, Max Brasen, Jens Christian Sorensen, Charlotte Mehlin |
| description | We investigated the mechanisms behind the endothelial-derived hyperpolarization (EDH)-induced renal vasodilation in vivo and in vitro in rats. We assessed the role of Ca
2+
-activated K
+
channels and whether K
+
released from the endothelial cells activates inward rectifier K
+
(K
ir
) channels and/or the Na
+
/K
+
-ATPase. Also, involvement of renal myoendothelial gap junctions was evaluated in vitro. Isometric tension in rat renal interlobar arteries was measured using a wire myograph. Renal blood flow was measured in isoflurane anesthetized rats. The EDH response was defined as the ACh-induced vasodilation assessed after inhibition of nitric oxide synthase and cyclooxygenase using L-NAME and indomethacin, respectively. After inhibition of small conductance Ca
2+
-activated K
+
channels (SK
Ca
) and intermediate conductance Ca
2+
-activated K
+
channels (IK
Ca
) (by apamin and TRAM-34, respectively), the EDH response in vitro was strongly attenuated whereas the EDH response in vivo was not significantly reduced. Inhibition of K
ir
channels and Na
+
/K
+
-ATPases (by ouabain and Ba
2+
, respectively) significantly attenuated renal vasorelaxation in vitro but did not affect the response in vivo. Inhibition of gap junctions in vitro using carbenoxolone or 18α-glycyrrhetinic acid significantly reduced the endothelial-derived hyperpolarization-induced vasorelaxation. We conclude that SK
Ca
and IK
Ca
channels are important for EDH-induced renal vasorelaxation in vitro. Activation of K
ir
channels and Na
+
/K
+
-ATPases plays a significant role in the renal vascular EDH response in vitro but not in vivo. The renal EDH response in vivo is complex and may consist of several overlapping mechanisms some of which remain obscure. |
| doi_str_mv | 10.1007/s00424-016-1805-x |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1804857794</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1804857794</sourcerecordid><originalsourceid>FETCH-LOGICAL-c410t-15a997e500344adce05678026481a641ae2bab0032b903b27245d4a0762d79743</originalsourceid><addsrcrecordid>eNp9kE1P4zAQhi0Egi7wA7ggH1dChrHj2MkRVcCuFokLnC0ndqmr1C52UlF-PQ4pe-Q0o3k_pHkQuqBwTQHkTQLgjBOggtAKSvJ-gGaUF4wwoMUhmgEUlAgpqhP0K6UVADBesWN0wkQtSsrFDO3mwffRNUPvgsdhgf9d4Xapvbddwn3A1pvQL23nhjUxNrqtNXi524ROR_ehxxBx3gxtPkfrdYe3OgXjui8JO4-j7tM4t24bsPZm2vsYztDRQnfJnu_nKXq5v3ue_yGPTw9_57ePpOUUekJLXdfSlvkXzrVpLZRCVsAEr6gWnGrLGt1klTU1FA2TjJeGa5CCGVlLXpyi31PvJoa3waZerV1qbddpb8OQVCbHq1LKerTSydrGkFK0C7WJbq3jTlFQI3E1EVeZ-Jgr1XvOXO7rh2Ztzf_EN-JsYJMhZcm_2qhWYYgZVfqh9RPy1ozp</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1804857794</pqid></control><display><type>article</type><title>Contribution of K+ channels to endothelium-derived hypolarization-induced renal vasodilation in rats in vivo and in vitro</title><source>MEDLINE</source><source>SpringerNature Journals</source><creator>Rasmussen, Kasper Moller Boje ; Braunstein, Thomas Hartig ; Salomonsson, Max ; Brasen, Jens Christian ; Sorensen, Charlotte Mehlin</creator><creatorcontrib>Rasmussen, Kasper Moller Boje ; Braunstein, Thomas Hartig ; Salomonsson, Max ; Brasen, Jens Christian ; Sorensen, Charlotte Mehlin</creatorcontrib><description>We investigated the mechanisms behind the endothelial-derived hyperpolarization (EDH)-induced renal vasodilation in vivo and in vitro in rats. We assessed the role of Ca
2+
-activated K
+
channels and whether K
+
released from the endothelial cells activates inward rectifier K
+
(K
ir
) channels and/or the Na
+
/K
+
-ATPase. Also, involvement of renal myoendothelial gap junctions was evaluated in vitro. Isometric tension in rat renal interlobar arteries was measured using a wire myograph. Renal blood flow was measured in isoflurane anesthetized rats. The EDH response was defined as the ACh-induced vasodilation assessed after inhibition of nitric oxide synthase and cyclooxygenase using L-NAME and indomethacin, respectively. After inhibition of small conductance Ca
2+
-activated K
+
channels (SK
Ca
) and intermediate conductance Ca
2+
-activated K
+
channels (IK
Ca
) (by apamin and TRAM-34, respectively), the EDH response in vitro was strongly attenuated whereas the EDH response in vivo was not significantly reduced. Inhibition of K
ir
channels and Na
+
/K
+
-ATPases (by ouabain and Ba
2+
, respectively) significantly attenuated renal vasorelaxation in vitro but did not affect the response in vivo. Inhibition of gap junctions in vitro using carbenoxolone or 18α-glycyrrhetinic acid significantly reduced the endothelial-derived hyperpolarization-induced vasorelaxation. We conclude that SK
Ca
and IK
Ca
channels are important for EDH-induced renal vasorelaxation in vitro. Activation of K
ir
channels and Na
+
/K
+
-ATPases plays a significant role in the renal vascular EDH response in vitro but not in vivo. The renal EDH response in vivo is complex and may consist of several overlapping mechanisms some of which remain obscure.</description><identifier>ISSN: 0031-6768</identifier><identifier>EISSN: 1432-2013</identifier><identifier>DOI: 10.1007/s00424-016-1805-x</identifier><identifier>PMID: 26965146</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Acetylcholine - pharmacology ; Animals ; Biomedical and Life Sciences ; Biomedicine ; Carbenoxolone - pharmacology ; Cell Biology ; Endothelium, Vascular - drug effects ; Endothelium, Vascular - metabolism ; Gap Junctions - drug effects ; Gap Junctions - metabolism ; Glycyrrhetinic Acid - analogs & derivatives ; Glycyrrhetinic Acid - pharmacology ; Human Physiology ; Integrative Physiology ; Kidney - drug effects ; Kidney - metabolism ; Male ; Molecular Medicine ; Neurosciences ; NG-Nitroarginine Methyl Ester - pharmacology ; Nitric Oxide - metabolism ; Nitric Oxide Synthase - metabolism ; Potassium Channels, Calcium-Activated - metabolism ; Pyrazoles - pharmacology ; Rats ; Rats, Sprague-Dawley ; Receptors ; Renal Circulation - drug effects ; Renal Circulation - physiology ; Sodium-Potassium-Exchanging ATPase - metabolism ; Vasodilation - drug effects ; Vasodilation - physiology</subject><ispartof>Pflügers Archiv, 2016-07, Vol.468 (7), p.1139-1149</ispartof><rights>Springer-Verlag Berlin Heidelberg 2016</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c410t-15a997e500344adce05678026481a641ae2bab0032b903b27245d4a0762d79743</citedby><cites>FETCH-LOGICAL-c410t-15a997e500344adce05678026481a641ae2bab0032b903b27245d4a0762d79743</cites><orcidid>0000-0003-4446-6331</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00424-016-1805-x$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00424-016-1805-x$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>315,781,785,27928,27929,41492,42561,51323</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26965146$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Rasmussen, Kasper Moller Boje</creatorcontrib><creatorcontrib>Braunstein, Thomas Hartig</creatorcontrib><creatorcontrib>Salomonsson, Max</creatorcontrib><creatorcontrib>Brasen, Jens Christian</creatorcontrib><creatorcontrib>Sorensen, Charlotte Mehlin</creatorcontrib><title>Contribution of K+ channels to endothelium-derived hypolarization-induced renal vasodilation in rats in vivo and in vitro</title><title>Pflügers Archiv</title><addtitle>Pflugers Arch - Eur J Physiol</addtitle><addtitle>Pflugers Arch</addtitle><description>We investigated the mechanisms behind the endothelial-derived hyperpolarization (EDH)-induced renal vasodilation in vivo and in vitro in rats. We assessed the role of Ca
2+
-activated K
+
channels and whether K
+
released from the endothelial cells activates inward rectifier K
+
(K
ir
) channels and/or the Na
+
/K
+
-ATPase. Also, involvement of renal myoendothelial gap junctions was evaluated in vitro. Isometric tension in rat renal interlobar arteries was measured using a wire myograph. Renal blood flow was measured in isoflurane anesthetized rats. The EDH response was defined as the ACh-induced vasodilation assessed after inhibition of nitric oxide synthase and cyclooxygenase using L-NAME and indomethacin, respectively. After inhibition of small conductance Ca
2+
-activated K
+
channels (SK
Ca
) and intermediate conductance Ca
2+
-activated K
+
channels (IK
Ca
) (by apamin and TRAM-34, respectively), the EDH response in vitro was strongly attenuated whereas the EDH response in vivo was not significantly reduced. Inhibition of K
ir
channels and Na
+
/K
+
-ATPases (by ouabain and Ba
2+
, respectively) significantly attenuated renal vasorelaxation in vitro but did not affect the response in vivo. Inhibition of gap junctions in vitro using carbenoxolone or 18α-glycyrrhetinic acid significantly reduced the endothelial-derived hyperpolarization-induced vasorelaxation. We conclude that SK
Ca
and IK
Ca
channels are important for EDH-induced renal vasorelaxation in vitro. Activation of K
ir
channels and Na
+
/K
+
-ATPases plays a significant role in the renal vascular EDH response in vitro but not in vivo. The renal EDH response in vivo is complex and may consist of several overlapping mechanisms some of which remain obscure.</description><subject>Acetylcholine - pharmacology</subject><subject>Animals</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Carbenoxolone - pharmacology</subject><subject>Cell Biology</subject><subject>Endothelium, Vascular - drug effects</subject><subject>Endothelium, Vascular - metabolism</subject><subject>Gap Junctions - drug effects</subject><subject>Gap Junctions - metabolism</subject><subject>Glycyrrhetinic Acid - analogs & derivatives</subject><subject>Glycyrrhetinic Acid - pharmacology</subject><subject>Human Physiology</subject><subject>Integrative Physiology</subject><subject>Kidney - drug effects</subject><subject>Kidney - metabolism</subject><subject>Male</subject><subject>Molecular Medicine</subject><subject>Neurosciences</subject><subject>NG-Nitroarginine Methyl Ester - pharmacology</subject><subject>Nitric Oxide - metabolism</subject><subject>Nitric Oxide Synthase - metabolism</subject><subject>Potassium Channels, Calcium-Activated - metabolism</subject><subject>Pyrazoles - pharmacology</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Receptors</subject><subject>Renal Circulation - drug effects</subject><subject>Renal Circulation - physiology</subject><subject>Sodium-Potassium-Exchanging ATPase - metabolism</subject><subject>Vasodilation - drug effects</subject><subject>Vasodilation - physiology</subject><issn>0031-6768</issn><issn>1432-2013</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kE1P4zAQhi0Egi7wA7ggH1dChrHj2MkRVcCuFokLnC0ndqmr1C52UlF-PQ4pe-Q0o3k_pHkQuqBwTQHkTQLgjBOggtAKSvJ-gGaUF4wwoMUhmgEUlAgpqhP0K6UVADBesWN0wkQtSsrFDO3mwffRNUPvgsdhgf9d4Xapvbddwn3A1pvQL23nhjUxNrqtNXi524ROR_ehxxBx3gxtPkfrdYe3OgXjui8JO4-j7tM4t24bsPZm2vsYztDRQnfJnu_nKXq5v3ue_yGPTw9_57ePpOUUekJLXdfSlvkXzrVpLZRCVsAEr6gWnGrLGt1klTU1FA2TjJeGa5CCGVlLXpyi31PvJoa3waZerV1qbddpb8OQVCbHq1LKerTSydrGkFK0C7WJbq3jTlFQI3E1EVeZ-Jgr1XvOXO7rh2Ztzf_EN-JsYJMhZcm_2qhWYYgZVfqh9RPy1ozp</recordid><startdate>20160701</startdate><enddate>20160701</enddate><creator>Rasmussen, Kasper Moller Boje</creator><creator>Braunstein, Thomas Hartig</creator><creator>Salomonsson, Max</creator><creator>Brasen, Jens Christian</creator><creator>Sorensen, Charlotte Mehlin</creator><general>Springer Berlin Heidelberg</general><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><orcidid>https://orcid.org/0000-0003-4446-6331</orcidid></search><sort><creationdate>20160701</creationdate><title>Contribution of K+ channels to endothelium-derived hypolarization-induced renal vasodilation in rats in vivo and in vitro</title><author>Rasmussen, Kasper Moller Boje ; Braunstein, Thomas Hartig ; Salomonsson, Max ; Brasen, Jens Christian ; Sorensen, Charlotte Mehlin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c410t-15a997e500344adce05678026481a641ae2bab0032b903b27245d4a0762d79743</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Acetylcholine - pharmacology</topic><topic>Animals</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Carbenoxolone - pharmacology</topic><topic>Cell Biology</topic><topic>Endothelium, Vascular - drug effects</topic><topic>Endothelium, Vascular - metabolism</topic><topic>Gap Junctions - drug effects</topic><topic>Gap Junctions - metabolism</topic><topic>Glycyrrhetinic Acid - analogs & derivatives</topic><topic>Glycyrrhetinic Acid - pharmacology</topic><topic>Human Physiology</topic><topic>Integrative Physiology</topic><topic>Kidney - drug effects</topic><topic>Kidney - metabolism</topic><topic>Male</topic><topic>Molecular Medicine</topic><topic>Neurosciences</topic><topic>NG-Nitroarginine Methyl Ester - pharmacology</topic><topic>Nitric Oxide - metabolism</topic><topic>Nitric Oxide Synthase - metabolism</topic><topic>Potassium Channels, Calcium-Activated - metabolism</topic><topic>Pyrazoles - pharmacology</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Receptors</topic><topic>Renal Circulation - drug effects</topic><topic>Renal Circulation - physiology</topic><topic>Sodium-Potassium-Exchanging ATPase - metabolism</topic><topic>Vasodilation - drug effects</topic><topic>Vasodilation - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Rasmussen, Kasper Moller Boje</creatorcontrib><creatorcontrib>Braunstein, Thomas Hartig</creatorcontrib><creatorcontrib>Salomonsson, Max</creatorcontrib><creatorcontrib>Brasen, Jens Christian</creatorcontrib><creatorcontrib>Sorensen, Charlotte Mehlin</creatorcontrib><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>Pflügers Archiv</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Rasmussen, Kasper Moller Boje</au><au>Braunstein, Thomas Hartig</au><au>Salomonsson, Max</au><au>Brasen, Jens Christian</au><au>Sorensen, Charlotte Mehlin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Contribution of K+ channels to endothelium-derived hypolarization-induced renal vasodilation in rats in vivo and in vitro</atitle><jtitle>Pflügers Archiv</jtitle><stitle>Pflugers Arch - Eur J Physiol</stitle><addtitle>Pflugers Arch</addtitle><date>2016-07-01</date><risdate>2016</risdate><volume>468</volume><issue>7</issue><spage>1139</spage><epage>1149</epage><pages>1139-1149</pages><issn>0031-6768</issn><eissn>1432-2013</eissn><abstract>We investigated the mechanisms behind the endothelial-derived hyperpolarization (EDH)-induced renal vasodilation in vivo and in vitro in rats. We assessed the role of Ca
2+
-activated K
+
channels and whether K
+
released from the endothelial cells activates inward rectifier K
+
(K
ir
) channels and/or the Na
+
/K
+
-ATPase. Also, involvement of renal myoendothelial gap junctions was evaluated in vitro. Isometric tension in rat renal interlobar arteries was measured using a wire myograph. Renal blood flow was measured in isoflurane anesthetized rats. The EDH response was defined as the ACh-induced vasodilation assessed after inhibition of nitric oxide synthase and cyclooxygenase using L-NAME and indomethacin, respectively. After inhibition of small conductance Ca
2+
-activated K
+
channels (SK
Ca
) and intermediate conductance Ca
2+
-activated K
+
channels (IK
Ca
) (by apamin and TRAM-34, respectively), the EDH response in vitro was strongly attenuated whereas the EDH response in vivo was not significantly reduced. Inhibition of K
ir
channels and Na
+
/K
+
-ATPases (by ouabain and Ba
2+
, respectively) significantly attenuated renal vasorelaxation in vitro but did not affect the response in vivo. Inhibition of gap junctions in vitro using carbenoxolone or 18α-glycyrrhetinic acid significantly reduced the endothelial-derived hyperpolarization-induced vasorelaxation. We conclude that SK
Ca
and IK
Ca
channels are important for EDH-induced renal vasorelaxation in vitro. Activation of K
ir
channels and Na
+
/K
+
-ATPases plays a significant role in the renal vascular EDH response in vitro but not in vivo. The renal EDH response in vivo is complex and may consist of several overlapping mechanisms some of which remain obscure.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><pmid>26965146</pmid><doi>10.1007/s00424-016-1805-x</doi><tpages>11</tpages><orcidid>https://orcid.org/0000-0003-4446-6331</orcidid></addata></record> |
| fulltext | fulltext |
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| ispartof | Pflügers Archiv, 2016-07, Vol.468 (7), p.1139-1149 |
| issn | 0031-6768 1432-2013 |
| language | eng |
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| source | MEDLINE; SpringerNature Journals |
| subjects | Acetylcholine - pharmacology Animals Biomedical and Life Sciences Biomedicine Carbenoxolone - pharmacology Cell Biology Endothelium, Vascular - drug effects Endothelium, Vascular - metabolism Gap Junctions - drug effects Gap Junctions - metabolism Glycyrrhetinic Acid - analogs & derivatives Glycyrrhetinic Acid - pharmacology Human Physiology Integrative Physiology Kidney - drug effects Kidney - metabolism Male Molecular Medicine Neurosciences NG-Nitroarginine Methyl Ester - pharmacology Nitric Oxide - metabolism Nitric Oxide Synthase - metabolism Potassium Channels, Calcium-Activated - metabolism Pyrazoles - pharmacology Rats Rats, Sprague-Dawley Receptors Renal Circulation - drug effects Renal Circulation - physiology Sodium-Potassium-Exchanging ATPase - metabolism Vasodilation - drug effects Vasodilation - physiology |
| title | Contribution of K+ channels to endothelium-derived hypolarization-induced renal vasodilation in rats in vivo and in vitro |
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