Iloprost dilates rat small arteries: role of K(ATP)- and K(Ca)-channel activation by cAMP-dependent protein kinase
R. Schubert, V. N. Serebryakov, H. Mewes and H. H. Hopp Faculty of Medicine, University of Rostock, Germany. The effect of the stable prostacyclin analog iloprost and its mechanism of action were investigated with the use of pressurized rat tail small arteries with a spontaneous myogenic tone. Ilopr...
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| Veröffentlicht in: | American journal of physiology. Heart and circulatory physiology 1997-03, Vol.272 (3), p.H1147-H1156 |
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| container_title | American journal of physiology. Heart and circulatory physiology |
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| creator | Schubert, R Serebryakov, V. N Mewes, H Hopp, H. H |
| description | R. Schubert, V. N. Serebryakov, H. Mewes and H. H. Hopp
Faculty of Medicine, University of Rostock, Germany.
The effect of the stable prostacyclin analog iloprost and its mechanism of
action were investigated with the use of pressurized rat tail small
arteries with a spontaneous myogenic tone. Iloprost concentration
dependently dilated these vessels with a half-maximal effective dose of 5.0
+/- 0.5 x 10(-8) M. Application of 10(-7)-10(-6) M glibenclamide, a blocker
of ATP-sensitive potassium (K(ATP)) channels, inhibited the
iloprost-induced dilation. Glibenclamide did not affect the basal vessel
diameter. The application of 5 x 10(-5)-10(-3) M tetraethylammonium (TEA)
and 5 x 10(-9)-10(-7) M iberiotoxin, blockers of calcium-activated
potassium (K(Ca)) channels, decreased vessel diameter in the presence of
iloprost. Both TEA and iberiotoxin reduced the basal vessel diameter.
Glibenclamide at 10(-6) M inhibited the dilation produced by 5 x 10(-5) M
Sp-5,6-DCl-cBIMPS, an activator of adenosine 3',5'-cyclic monophosphate
(cAMP)-dependent protein kinase. Iberiotoxin at 10(-7) M decreased vessel
diameter in the presence of Sp-5,6-DCl-cBIMPS. H-89 and Rp-8-CPT-cAMPS,
blockers of cAMP-dependent protein kinase A (PKA), inhibited the
iloprost-induced dilation of these vessels. With use of the whole cell
configuration of the patch-clamp technique, it was observed that 5 x 10(-7)
M iloprost enhanced an outward current, determined largely by K(Ca)
channels, 1.79 +/- 0.17-fold in freshly isolated smooth muscle cells from
rat tail small artery. These data show that iloprost dilates rat tail small
arteries with a spontaneous myogenic tone and suggest that K(ATP) as well
as K(Ca) channels are involved in this effect, which is mediated, at least
partly, by PKA. |
| doi_str_mv | 10.1152/ajpheart.1997.272.3.h1147 |
| format | Article |
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Faculty of Medicine, University of Rostock, Germany.
The effect of the stable prostacyclin analog iloprost and its mechanism of
action were investigated with the use of pressurized rat tail small
arteries with a spontaneous myogenic tone. Iloprost concentration
dependently dilated these vessels with a half-maximal effective dose of 5.0
+/- 0.5 x 10(-8) M. Application of 10(-7)-10(-6) M glibenclamide, a blocker
of ATP-sensitive potassium (K(ATP)) channels, inhibited the
iloprost-induced dilation. Glibenclamide did not affect the basal vessel
diameter. The application of 5 x 10(-5)-10(-3) M tetraethylammonium (TEA)
and 5 x 10(-9)-10(-7) M iberiotoxin, blockers of calcium-activated
potassium (K(Ca)) channels, decreased vessel diameter in the presence of
iloprost. Both TEA and iberiotoxin reduced the basal vessel diameter.
Glibenclamide at 10(-6) M inhibited the dilation produced by 5 x 10(-5) M
Sp-5,6-DCl-cBIMPS, an activator of adenosine 3',5'-cyclic monophosphate
(cAMP)-dependent protein kinase. Iberiotoxin at 10(-7) M decreased vessel
diameter in the presence of Sp-5,6-DCl-cBIMPS. H-89 and Rp-8-CPT-cAMPS,
blockers of cAMP-dependent protein kinase A (PKA), inhibited the
iloprost-induced dilation of these vessels. With use of the whole cell
configuration of the patch-clamp technique, it was observed that 5 x 10(-7)
M iloprost enhanced an outward current, determined largely by K(Ca)
channels, 1.79 +/- 0.17-fold in freshly isolated smooth muscle cells from
rat tail small artery. These data show that iloprost dilates rat tail small
arteries with a spontaneous myogenic tone and suggest that K(ATP) as well
as K(Ca) channels are involved in this effect, which is mediated, at least
partly, by PKA.</description><identifier>ISSN: 0363-6135</identifier><identifier>ISSN: 0002-9513</identifier><identifier>EISSN: 1522-1539</identifier><identifier>DOI: 10.1152/ajpheart.1997.272.3.h1147</identifier><identifier>PMID: 9087587</identifier><language>eng</language><publisher>United States</publisher><subject>Adenosine Triphosphate - pharmacology ; Animals ; Arteries - drug effects ; Arteries - physiology ; Calcium - pharmacology ; Cyclic AMP - analogs & derivatives ; Cyclic AMP - pharmacology ; Cyclic AMP-Dependent Protein Kinases - antagonists & inhibitors ; Cyclic AMP-Dependent Protein Kinases - metabolism ; Dichlororibofuranosylbenzimidazole - analogs & derivatives ; Dichlororibofuranosylbenzimidazole - pharmacology ; Enzyme Inhibitors - pharmacology ; Glyburide - pharmacology ; Iloprost - pharmacology ; In Vitro Techniques ; Kinetics ; Male ; Muscle, Smooth, Vascular - drug effects ; Muscle, Smooth, Vascular - physiology ; Peptides - pharmacology ; Potassium Channels - drug effects ; Potassium Channels - physiology ; Rats ; Rats, Inbred WKY ; Scorpion Venoms - pharmacology ; Tail - blood supply ; Tetraethylammonium ; Tetraethylammonium Compounds - pharmacology ; Thionucleotides - pharmacology ; Vasoconstriction ; Vasodilation - drug effects</subject><ispartof>American journal of physiology. Heart and circulatory physiology, 1997-03, Vol.272 (3), p.H1147-H1156</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c333t-556a4779bfb13de204baae25f06fef7085c04efee3fdb6f5b0bddb94af7d96a93</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,3039,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9087587$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Schubert, R</creatorcontrib><creatorcontrib>Serebryakov, V. N</creatorcontrib><creatorcontrib>Mewes, H</creatorcontrib><creatorcontrib>Hopp, H. H</creatorcontrib><title>Iloprost dilates rat small arteries: role of K(ATP)- and K(Ca)-channel activation by cAMP-dependent protein kinase</title><title>American journal of physiology. Heart and circulatory physiology</title><addtitle>Am J Physiol</addtitle><description>R. Schubert, V. N. Serebryakov, H. Mewes and H. H. Hopp
Faculty of Medicine, University of Rostock, Germany.
The effect of the stable prostacyclin analog iloprost and its mechanism of
action were investigated with the use of pressurized rat tail small
arteries with a spontaneous myogenic tone. Iloprost concentration
dependently dilated these vessels with a half-maximal effective dose of 5.0
+/- 0.5 x 10(-8) M. Application of 10(-7)-10(-6) M glibenclamide, a blocker
of ATP-sensitive potassium (K(ATP)) channels, inhibited the
iloprost-induced dilation. Glibenclamide did not affect the basal vessel
diameter. The application of 5 x 10(-5)-10(-3) M tetraethylammonium (TEA)
and 5 x 10(-9)-10(-7) M iberiotoxin, blockers of calcium-activated
potassium (K(Ca)) channels, decreased vessel diameter in the presence of
iloprost. Both TEA and iberiotoxin reduced the basal vessel diameter.
Glibenclamide at 10(-6) M inhibited the dilation produced by 5 x 10(-5) M
Sp-5,6-DCl-cBIMPS, an activator of adenosine 3',5'-cyclic monophosphate
(cAMP)-dependent protein kinase. Iberiotoxin at 10(-7) M decreased vessel
diameter in the presence of Sp-5,6-DCl-cBIMPS. H-89 and Rp-8-CPT-cAMPS,
blockers of cAMP-dependent protein kinase A (PKA), inhibited the
iloprost-induced dilation of these vessels. With use of the whole cell
configuration of the patch-clamp technique, it was observed that 5 x 10(-7)
M iloprost enhanced an outward current, determined largely by K(Ca)
channels, 1.79 +/- 0.17-fold in freshly isolated smooth muscle cells from
rat tail small artery. These data show that iloprost dilates rat tail small
arteries with a spontaneous myogenic tone and suggest that K(ATP) as well
as K(Ca) channels are involved in this effect, which is mediated, at least
partly, by PKA.</description><subject>Adenosine Triphosphate - pharmacology</subject><subject>Animals</subject><subject>Arteries - drug effects</subject><subject>Arteries - physiology</subject><subject>Calcium - pharmacology</subject><subject>Cyclic AMP - analogs & derivatives</subject><subject>Cyclic AMP - pharmacology</subject><subject>Cyclic AMP-Dependent Protein Kinases - antagonists & inhibitors</subject><subject>Cyclic AMP-Dependent Protein Kinases - metabolism</subject><subject>Dichlororibofuranosylbenzimidazole - analogs & derivatives</subject><subject>Dichlororibofuranosylbenzimidazole - pharmacology</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>Glyburide - pharmacology</subject><subject>Iloprost - pharmacology</subject><subject>In Vitro Techniques</subject><subject>Kinetics</subject><subject>Male</subject><subject>Muscle, Smooth, Vascular - drug effects</subject><subject>Muscle, Smooth, Vascular - physiology</subject><subject>Peptides - pharmacology</subject><subject>Potassium Channels - drug effects</subject><subject>Potassium Channels - physiology</subject><subject>Rats</subject><subject>Rats, Inbred WKY</subject><subject>Scorpion Venoms - pharmacology</subject><subject>Tail - blood supply</subject><subject>Tetraethylammonium</subject><subject>Tetraethylammonium Compounds - pharmacology</subject><subject>Thionucleotides - pharmacology</subject><subject>Vasoconstriction</subject><subject>Vasodilation - drug effects</subject><issn>0363-6135</issn><issn>0002-9513</issn><issn>1522-1539</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1997</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpNkE1v2yAYx9G0qsvafYRJ7DKtB7tgjAm7RdG6VmvVHrozwuahpiPYA7Ip375EyV5OzyP936QfQh8oqSnlzaV-nkfQMddUSlE3oqlZPVLaildoUfSmopzJ12hBWMeqjjL-Br1N6ZkQwkXHTtGpJEvBl2KB4o2f5jiljI3zOkPCUWecNtp7XAYgOkifcZw84Mnib59Wjw8XFdbBlH-tL6ph1CFA8Q7Z_dLZTQH3Ozys7h4qAzMEAyHjMpDBBfzDBZ3gHJ1Y7RO8O94z9P3qy-P6urq9_3qzXt1WA2MsV5x3uhVC9ranzEBD2l5raLglnQUryJIPpAULwKzpO8t70hvTy1ZbYWSnJTtDHw-9Zf7nFlJWG5cG8F4HmLZJiaUksoAoRnkwDgVEimDVHN1Gx52iRO15qz-81Z63KrwVU9d73iX7_jiy7Tdg_iaPgIt-edBH9zT-dhHUPO6Sm_z0tPtX-3_jC4JJkQI</recordid><startdate>199703</startdate><enddate>199703</enddate><creator>Schubert, R</creator><creator>Serebryakov, V. N</creator><creator>Mewes, H</creator><creator>Hopp, H. H</creator><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>199703</creationdate><title>Iloprost dilates rat small arteries: role of K(ATP)- and K(Ca)-channel activation by cAMP-dependent protein kinase</title><author>Schubert, R ; Serebryakov, V. N ; Mewes, H ; Hopp, H. H</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c333t-556a4779bfb13de204baae25f06fef7085c04efee3fdb6f5b0bddb94af7d96a93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1997</creationdate><topic>Adenosine Triphosphate - pharmacology</topic><topic>Animals</topic><topic>Arteries - drug effects</topic><topic>Arteries - physiology</topic><topic>Calcium - pharmacology</topic><topic>Cyclic AMP - analogs & derivatives</topic><topic>Cyclic AMP - pharmacology</topic><topic>Cyclic AMP-Dependent Protein Kinases - antagonists & inhibitors</topic><topic>Cyclic AMP-Dependent Protein Kinases - metabolism</topic><topic>Dichlororibofuranosylbenzimidazole - analogs & derivatives</topic><topic>Dichlororibofuranosylbenzimidazole - pharmacology</topic><topic>Enzyme Inhibitors - pharmacology</topic><topic>Glyburide - pharmacology</topic><topic>Iloprost - pharmacology</topic><topic>In Vitro Techniques</topic><topic>Kinetics</topic><topic>Male</topic><topic>Muscle, Smooth, Vascular - drug effects</topic><topic>Muscle, Smooth, Vascular - physiology</topic><topic>Peptides - pharmacology</topic><topic>Potassium Channels - drug effects</topic><topic>Potassium Channels - physiology</topic><topic>Rats</topic><topic>Rats, Inbred WKY</topic><topic>Scorpion Venoms - pharmacology</topic><topic>Tail - blood supply</topic><topic>Tetraethylammonium</topic><topic>Tetraethylammonium Compounds - pharmacology</topic><topic>Thionucleotides - pharmacology</topic><topic>Vasoconstriction</topic><topic>Vasodilation - drug effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Schubert, R</creatorcontrib><creatorcontrib>Serebryakov, V. N</creatorcontrib><creatorcontrib>Mewes, H</creatorcontrib><creatorcontrib>Hopp, H. H</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>American journal of physiology. Heart and circulatory physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Schubert, R</au><au>Serebryakov, V. N</au><au>Mewes, H</au><au>Hopp, H. H</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Iloprost dilates rat small arteries: role of K(ATP)- and K(Ca)-channel activation by cAMP-dependent protein kinase</atitle><jtitle>American journal of physiology. Heart and circulatory physiology</jtitle><addtitle>Am J Physiol</addtitle><date>1997-03</date><risdate>1997</risdate><volume>272</volume><issue>3</issue><spage>H1147</spage><epage>H1156</epage><pages>H1147-H1156</pages><issn>0363-6135</issn><issn>0002-9513</issn><eissn>1522-1539</eissn><abstract>R. Schubert, V. N. Serebryakov, H. Mewes and H. H. Hopp
Faculty of Medicine, University of Rostock, Germany.
The effect of the stable prostacyclin analog iloprost and its mechanism of
action were investigated with the use of pressurized rat tail small
arteries with a spontaneous myogenic tone. Iloprost concentration
dependently dilated these vessels with a half-maximal effective dose of 5.0
+/- 0.5 x 10(-8) M. Application of 10(-7)-10(-6) M glibenclamide, a blocker
of ATP-sensitive potassium (K(ATP)) channels, inhibited the
iloprost-induced dilation. Glibenclamide did not affect the basal vessel
diameter. The application of 5 x 10(-5)-10(-3) M tetraethylammonium (TEA)
and 5 x 10(-9)-10(-7) M iberiotoxin, blockers of calcium-activated
potassium (K(Ca)) channels, decreased vessel diameter in the presence of
iloprost. Both TEA and iberiotoxin reduced the basal vessel diameter.
Glibenclamide at 10(-6) M inhibited the dilation produced by 5 x 10(-5) M
Sp-5,6-DCl-cBIMPS, an activator of adenosine 3',5'-cyclic monophosphate
(cAMP)-dependent protein kinase. Iberiotoxin at 10(-7) M decreased vessel
diameter in the presence of Sp-5,6-DCl-cBIMPS. H-89 and Rp-8-CPT-cAMPS,
blockers of cAMP-dependent protein kinase A (PKA), inhibited the
iloprost-induced dilation of these vessels. With use of the whole cell
configuration of the patch-clamp technique, it was observed that 5 x 10(-7)
M iloprost enhanced an outward current, determined largely by K(Ca)
channels, 1.79 +/- 0.17-fold in freshly isolated smooth muscle cells from
rat tail small artery. These data show that iloprost dilates rat tail small
arteries with a spontaneous myogenic tone and suggest that K(ATP) as well
as K(Ca) channels are involved in this effect, which is mediated, at least
partly, by PKA.</abstract><cop>United States</cop><pmid>9087587</pmid><doi>10.1152/ajpheart.1997.272.3.h1147</doi></addata></record> |
| fulltext | fulltext |
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| ispartof | American journal of physiology. Heart and circulatory physiology, 1997-03, Vol.272 (3), p.H1147-H1156 |
| issn | 0363-6135 0002-9513 1522-1539 |
| language | eng |
| recordid | cdi_highwire_physiology_ajpheart_272_3_H1147 |
| source | MEDLINE; American Physiological Society Paid; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Adenosine Triphosphate - pharmacology Animals Arteries - drug effects Arteries - physiology Calcium - pharmacology Cyclic AMP - analogs & derivatives Cyclic AMP - pharmacology Cyclic AMP-Dependent Protein Kinases - antagonists & inhibitors Cyclic AMP-Dependent Protein Kinases - metabolism Dichlororibofuranosylbenzimidazole - analogs & derivatives Dichlororibofuranosylbenzimidazole - pharmacology Enzyme Inhibitors - pharmacology Glyburide - pharmacology Iloprost - pharmacology In Vitro Techniques Kinetics Male Muscle, Smooth, Vascular - drug effects Muscle, Smooth, Vascular - physiology Peptides - pharmacology Potassium Channels - drug effects Potassium Channels - physiology Rats Rats, Inbred WKY Scorpion Venoms - pharmacology Tail - blood supply Tetraethylammonium Tetraethylammonium Compounds - pharmacology Thionucleotides - pharmacology Vasoconstriction Vasodilation - drug effects |
| title | Iloprost dilates rat small arteries: role of K(ATP)- and K(Ca)-channel activation by cAMP-dependent protein kinase |
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