K+ is an endothelium-derived hyperpolarizing factor in rat arteries
In arteries, muscarinic agonists such as acetylcholine release an unidentified, endothelium-derived hyperpolarizing factor (EDHF) which is neither prostacyclin nor nitric oxide 1 , 2 , 3 . Here we show that EDHF-induced hyperpolarization of smooth muscle and relaxation of small resistance arteries a...
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| Veröffentlicht in: | Nature (London) 1998-11, Vol.396 (6708), p.269-272 |
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| creator | Edwards, G. Dora, K. A. Gardener, M. J. Garland, C. J. Weston, A. H. |
| description | In arteries, muscarinic agonists such as acetylcholine release an unidentified, endothelium-derived hyperpolarizing factor (EDHF) which is neither prostacyclin nor nitric oxide
1
,
2
,
3
. Here we show that EDHF-induced hyperpolarization of smooth muscle and relaxation of small resistance arteries are inhibited by ouabain plus Ba
2+
; ouabain is a blocker of Na
+
/K
+
ATPase
4
and Ba
2+
blocks inwardly rectifying K
+
channels
5
. Small increases in the amount of extracellular K
+
mimic these effects of EDHF in a ouabain- and Ba
2+
-sensitive, but endothelium-independent, manner. Acetylcholine hyperpolarizes endothelial cells and increases the K
+
concentration in the myoendothelial space; these effects are abolished by charbdotoxin plus apamin. Hyperpolarization of smooth muscle by EDHF is also abolished by this toxin combination, but these toxins do not affect the hyperpolarizaiton of smooth muscle by added K
+
. These data show that EDHF is K
+
that effluxes through charybdotoxin- and apamin-sensitive K
+
channels on endothelial cells. The resulting increase in myoendothelial K
+
concentration hyperpolarizes and relaxes adjacent smooth-muscle cells by activating Ba
2+
-sensitive K
+
channels and Na
+
/K
+
ATPase. These results show that fluctuations in K
+
levels originating within the blood vessel itself are important in regulating mammalian blood pressure and flow. |
| doi_str_mv | 10.1038/24388 |
| format | Article |
| fullrecord | <record><control><sourceid>pubmed_cross</sourceid><recordid>TN_cdi_crossref_primary_10_1038_24388</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>9834033</sourcerecordid><originalsourceid>FETCH-LOGICAL-c332t-aca52a76c7daa606f4428546b54db0042c3e3b020a4eb306098323afd950b06e3</originalsourceid><addsrcrecordid>eNpdkM1OwzAQhC0EKqX0EZB8AC4osLEdxzmiij9RiQuco43jtK5SJ7JTpPbpMbQCidMe5tPMzhAyTeE2Ba7umOBKHZFxKnKZCKnyYzIGYCoBxeUpOQthBQBZmosRGRWKC-B8TGavN9QGio4aV3fD0rR2s05q4-2nqely2xvfdy16u7NuQRvUQ-epddTjQNEPkTPhnJw02AYzPdwJ-Xh8eJ89J_O3p5fZ_TzRnLMhQY0Zw1zqvEaUIBshmMqErDJRVwCCaW54BQxQmIqDhPgk49jURQYVSMMn5Grvq30XgjdN2Xu7Rr8tUyi_Nyh_NojcxZ7rN9Xa1L_UoXTULw86Bo1t49FpG_7MsgJAFhG73mMhKm5hfLnqNt7Fhv_yvgBEj24l</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype></control><display><type>article</type><title>K+ is an endothelium-derived hyperpolarizing factor in rat arteries</title><source>MEDLINE</source><source>Springer Nature - Complete Springer Journals</source><source>Nature</source><creator>Edwards, G. ; Dora, K. A. ; Gardener, M. J. ; Garland, C. J. ; Weston, A. H.</creator><creatorcontrib>Edwards, G. ; Dora, K. A. ; Gardener, M. J. ; Garland, C. J. ; Weston, A. H.</creatorcontrib><description>In arteries, muscarinic agonists such as acetylcholine release an unidentified, endothelium-derived hyperpolarizing factor (EDHF) which is neither prostacyclin nor nitric oxide
1
,
2
,
3
. Here we show that EDHF-induced hyperpolarization of smooth muscle and relaxation of small resistance arteries are inhibited by ouabain plus Ba
2+
; ouabain is a blocker of Na
+
/K
+
ATPase
4
and Ba
2+
blocks inwardly rectifying K
+
channels
5
. Small increases in the amount of extracellular K
+
mimic these effects of EDHF in a ouabain- and Ba
2+
-sensitive, but endothelium-independent, manner. Acetylcholine hyperpolarizes endothelial cells and increases the K
+
concentration in the myoendothelial space; these effects are abolished by charbdotoxin plus apamin. Hyperpolarization of smooth muscle by EDHF is also abolished by this toxin combination, but these toxins do not affect the hyperpolarizaiton of smooth muscle by added K
+
. These data show that EDHF is K
+
that effluxes through charybdotoxin- and apamin-sensitive K
+
channels on endothelial cells. The resulting increase in myoendothelial K
+
concentration hyperpolarizes and relaxes adjacent smooth-muscle cells by activating Ba
2+
-sensitive K
+
channels and Na
+
/K
+
ATPase. These results show that fluctuations in K
+
levels originating within the blood vessel itself are important in regulating mammalian blood pressure and flow.</description><identifier>ISSN: 0028-0836</identifier><identifier>EISSN: 1476-4687</identifier><identifier>DOI: 10.1038/24388</identifier><identifier>PMID: 9834033</identifier><identifier>CODEN: NATUAS</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>Acetylcholine - pharmacology ; Animals ; Apamin - pharmacology ; Arteries - drug effects ; Arteries - physiology ; Barium - pharmacology ; Biological and medical sciences ; Biological Factors - metabolism ; Biological Factors - physiology ; Blood vessels and receptors ; Charybdotoxin - pharmacology ; Endothelium, Vascular - drug effects ; Endothelium, Vascular - physiology ; Enzyme Inhibitors - pharmacology ; Fundamental and applied biological sciences. Psychology ; Hepatic Artery ; Humanities and Social Sciences ; In Vitro Techniques ; letter ; Male ; Membrane Potentials ; multidisciplinary ; Muscle, Smooth, Vascular - drug effects ; Muscle, Smooth, Vascular - physiology ; Ouabain - pharmacology ; Patch-Clamp Techniques ; Potassium - metabolism ; Potassium - physiology ; Potassium Channel Blockers ; Potassium Channels - metabolism ; Rats ; Rats, Sprague-Dawley ; Science ; Science (multidisciplinary) ; Sodium-Potassium-Exchanging ATPase - antagonists & inhibitors ; Sodium-Potassium-Exchanging ATPase - metabolism ; Vasodilation - drug effects ; Vasodilation - physiology ; Vertebrates: cardiovascular system</subject><ispartof>Nature (London), 1998-11, Vol.396 (6708), p.269-272</ispartof><rights>Macmillan Magazines Ltd. 1998</rights><rights>1999 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c332t-aca52a76c7daa606f4428546b54db0042c3e3b020a4eb306098323afd950b06e3</citedby><cites>FETCH-LOGICAL-c332t-aca52a76c7daa606f4428546b54db0042c3e3b020a4eb306098323afd950b06e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/24388$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/24388$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1590069$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9834033$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Edwards, G.</creatorcontrib><creatorcontrib>Dora, K. A.</creatorcontrib><creatorcontrib>Gardener, M. J.</creatorcontrib><creatorcontrib>Garland, C. J.</creatorcontrib><creatorcontrib>Weston, A. H.</creatorcontrib><title>K+ is an endothelium-derived hyperpolarizing factor in rat arteries</title><title>Nature (London)</title><addtitle>Nature</addtitle><addtitle>Nature</addtitle><description>In arteries, muscarinic agonists such as acetylcholine release an unidentified, endothelium-derived hyperpolarizing factor (EDHF) which is neither prostacyclin nor nitric oxide
1
,
2
,
3
. Here we show that EDHF-induced hyperpolarization of smooth muscle and relaxation of small resistance arteries are inhibited by ouabain plus Ba
2+
; ouabain is a blocker of Na
+
/K
+
ATPase
4
and Ba
2+
blocks inwardly rectifying K
+
channels
5
. Small increases in the amount of extracellular K
+
mimic these effects of EDHF in a ouabain- and Ba
2+
-sensitive, but endothelium-independent, manner. Acetylcholine hyperpolarizes endothelial cells and increases the K
+
concentration in the myoendothelial space; these effects are abolished by charbdotoxin plus apamin. Hyperpolarization of smooth muscle by EDHF is also abolished by this toxin combination, but these toxins do not affect the hyperpolarizaiton of smooth muscle by added K
+
. These data show that EDHF is K
+
that effluxes through charybdotoxin- and apamin-sensitive K
+
channels on endothelial cells. The resulting increase in myoendothelial K
+
concentration hyperpolarizes and relaxes adjacent smooth-muscle cells by activating Ba
2+
-sensitive K
+
channels and Na
+
/K
+
ATPase. These results show that fluctuations in K
+
levels originating within the blood vessel itself are important in regulating mammalian blood pressure and flow.</description><subject>Acetylcholine - pharmacology</subject><subject>Animals</subject><subject>Apamin - pharmacology</subject><subject>Arteries - drug effects</subject><subject>Arteries - physiology</subject><subject>Barium - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Biological Factors - metabolism</subject><subject>Biological Factors - physiology</subject><subject>Blood vessels and receptors</subject><subject>Charybdotoxin - pharmacology</subject><subject>Endothelium, Vascular - drug effects</subject><subject>Endothelium, Vascular - physiology</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Hepatic Artery</subject><subject>Humanities and Social Sciences</subject><subject>In Vitro Techniques</subject><subject>letter</subject><subject>Male</subject><subject>Membrane Potentials</subject><subject>multidisciplinary</subject><subject>Muscle, Smooth, Vascular - drug effects</subject><subject>Muscle, Smooth, Vascular - physiology</subject><subject>Ouabain - pharmacology</subject><subject>Patch-Clamp Techniques</subject><subject>Potassium - metabolism</subject><subject>Potassium - physiology</subject><subject>Potassium Channel Blockers</subject><subject>Potassium Channels - metabolism</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Science</subject><subject>Science (multidisciplinary)</subject><subject>Sodium-Potassium-Exchanging ATPase - antagonists & inhibitors</subject><subject>Sodium-Potassium-Exchanging ATPase - metabolism</subject><subject>Vasodilation - drug effects</subject><subject>Vasodilation - physiology</subject><subject>Vertebrates: cardiovascular system</subject><issn>0028-0836</issn><issn>1476-4687</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkM1OwzAQhC0EKqX0EZB8AC4osLEdxzmiij9RiQuco43jtK5SJ7JTpPbpMbQCidMe5tPMzhAyTeE2Ba7umOBKHZFxKnKZCKnyYzIGYCoBxeUpOQthBQBZmosRGRWKC-B8TGavN9QGio4aV3fD0rR2s05q4-2nqely2xvfdy16u7NuQRvUQ-epddTjQNEPkTPhnJw02AYzPdwJ-Xh8eJ89J_O3p5fZ_TzRnLMhQY0Zw1zqvEaUIBshmMqErDJRVwCCaW54BQxQmIqDhPgk49jURQYVSMMn5Grvq30XgjdN2Xu7Rr8tUyi_Nyh_NojcxZ7rN9Xa1L_UoXTULw86Bo1t49FpG_7MsgJAFhG73mMhKm5hfLnqNt7Fhv_yvgBEj24l</recordid><startdate>19981119</startdate><enddate>19981119</enddate><creator>Edwards, G.</creator><creator>Dora, K. A.</creator><creator>Gardener, M. J.</creator><creator>Garland, C. J.</creator><creator>Weston, A. H.</creator><general>Nature Publishing Group UK</general><general>Nature Publishing</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></search><sort><creationdate>19981119</creationdate><title>K+ is an endothelium-derived hyperpolarizing factor in rat arteries</title><author>Edwards, G. ; Dora, K. A. ; Gardener, M. J. ; Garland, C. J. ; Weston, A. H.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c332t-aca52a76c7daa606f4428546b54db0042c3e3b020a4eb306098323afd950b06e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1998</creationdate><topic>Acetylcholine - pharmacology</topic><topic>Animals</topic><topic>Apamin - pharmacology</topic><topic>Arteries - drug effects</topic><topic>Arteries - physiology</topic><topic>Barium - pharmacology</topic><topic>Biological and medical sciences</topic><topic>Biological Factors - metabolism</topic><topic>Biological Factors - physiology</topic><topic>Blood vessels and receptors</topic><topic>Charybdotoxin - pharmacology</topic><topic>Endothelium, Vascular - drug effects</topic><topic>Endothelium, Vascular - physiology</topic><topic>Enzyme Inhibitors - pharmacology</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Hepatic Artery</topic><topic>Humanities and Social Sciences</topic><topic>In Vitro Techniques</topic><topic>letter</topic><topic>Male</topic><topic>Membrane Potentials</topic><topic>multidisciplinary</topic><topic>Muscle, Smooth, Vascular - drug effects</topic><topic>Muscle, Smooth, Vascular - physiology</topic><topic>Ouabain - pharmacology</topic><topic>Patch-Clamp Techniques</topic><topic>Potassium - metabolism</topic><topic>Potassium - physiology</topic><topic>Potassium Channel Blockers</topic><topic>Potassium Channels - metabolism</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Science</topic><topic>Science (multidisciplinary)</topic><topic>Sodium-Potassium-Exchanging ATPase - antagonists & inhibitors</topic><topic>Sodium-Potassium-Exchanging ATPase - metabolism</topic><topic>Vasodilation - drug effects</topic><topic>Vasodilation - physiology</topic><topic>Vertebrates: cardiovascular system</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Edwards, G.</creatorcontrib><creatorcontrib>Dora, K. A.</creatorcontrib><creatorcontrib>Gardener, M. J.</creatorcontrib><creatorcontrib>Garland, C. J.</creatorcontrib><creatorcontrib>Weston, A. H.</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><jtitle>Nature (London)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Edwards, G.</au><au>Dora, K. A.</au><au>Gardener, M. J.</au><au>Garland, C. J.</au><au>Weston, A. H.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>K+ is an endothelium-derived hyperpolarizing factor in rat arteries</atitle><jtitle>Nature (London)</jtitle><stitle>Nature</stitle><addtitle>Nature</addtitle><date>1998-11-19</date><risdate>1998</risdate><volume>396</volume><issue>6708</issue><spage>269</spage><epage>272</epage><pages>269-272</pages><issn>0028-0836</issn><eissn>1476-4687</eissn><coden>NATUAS</coden><abstract>In arteries, muscarinic agonists such as acetylcholine release an unidentified, endothelium-derived hyperpolarizing factor (EDHF) which is neither prostacyclin nor nitric oxide
1
,
2
,
3
. Here we show that EDHF-induced hyperpolarization of smooth muscle and relaxation of small resistance arteries are inhibited by ouabain plus Ba
2+
; ouabain is a blocker of Na
+
/K
+
ATPase
4
and Ba
2+
blocks inwardly rectifying K
+
channels
5
. Small increases in the amount of extracellular K
+
mimic these effects of EDHF in a ouabain- and Ba
2+
-sensitive, but endothelium-independent, manner. Acetylcholine hyperpolarizes endothelial cells and increases the K
+
concentration in the myoendothelial space; these effects are abolished by charbdotoxin plus apamin. Hyperpolarization of smooth muscle by EDHF is also abolished by this toxin combination, but these toxins do not affect the hyperpolarizaiton of smooth muscle by added K
+
. These data show that EDHF is K
+
that effluxes through charybdotoxin- and apamin-sensitive K
+
channels on endothelial cells. The resulting increase in myoendothelial K
+
concentration hyperpolarizes and relaxes adjacent smooth-muscle cells by activating Ba
2+
-sensitive K
+
channels and Na
+
/K
+
ATPase. These results show that fluctuations in K
+
levels originating within the blood vessel itself are important in regulating mammalian blood pressure and flow.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>9834033</pmid><doi>10.1038/24388</doi><tpages>4</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0028-0836 |
| ispartof | Nature (London), 1998-11, Vol.396 (6708), p.269-272 |
| issn | 0028-0836 1476-4687 |
| language | eng |
| recordid | cdi_crossref_primary_10_1038_24388 |
| source | MEDLINE; Springer Nature - Complete Springer Journals; Nature |
| subjects | Acetylcholine - pharmacology Animals Apamin - pharmacology Arteries - drug effects Arteries - physiology Barium - pharmacology Biological and medical sciences Biological Factors - metabolism Biological Factors - physiology Blood vessels and receptors Charybdotoxin - pharmacology Endothelium, Vascular - drug effects Endothelium, Vascular - physiology Enzyme Inhibitors - pharmacology Fundamental and applied biological sciences. Psychology Hepatic Artery Humanities and Social Sciences In Vitro Techniques letter Male Membrane Potentials multidisciplinary Muscle, Smooth, Vascular - drug effects Muscle, Smooth, Vascular - physiology Ouabain - pharmacology Patch-Clamp Techniques Potassium - metabolism Potassium - physiology Potassium Channel Blockers Potassium Channels - metabolism Rats Rats, Sprague-Dawley Science Science (multidisciplinary) Sodium-Potassium-Exchanging ATPase - antagonists & inhibitors Sodium-Potassium-Exchanging ATPase - metabolism Vasodilation - drug effects Vasodilation - physiology Vertebrates: cardiovascular system |
| title | K+ is an endothelium-derived hyperpolarizing factor in rat arteries |
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