Studies on the mechanism of action of the vasoconstrictive dihydropyridine, CGP 28392
The effects of the vasoconstrictive dihydropyridine, CGP 29392, upon tension development and 45Ca 2+ uptake by vascular smooth muscle were studied using isolated rabbit aorta. CGP 28392 did not elicit contractile responses when administered alone but lowered the threshold for the contractile respons...
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| Veröffentlicht in: | European journal of pharmacology 1984-10, Vol.105 (3), p.229-237 |
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| creator | Loutzenhiser, Rodger Rüegg, Urs T. Hof, Akiko Hof, Robert P. |
| description | The effects of the vasoconstrictive dihydropyridine, CGP 29392, upon tension development and
45Ca
2+ uptake by vascular smooth muscle were studied using isolated rabbit aorta. CGP 28392 did not elicit contractile responses when administered alone but lowered the threshold for the contractile response to elevated extracellular K
+. CGP 28392 also increased the magnitude of the contractions elicited by submaximal concentrations of K
+. This effect was competitively antagonized by PY 108-068, a Ca antagonist of the dihydropyridine class. Similarly, the relaxing effects of PY 108-068 upon KCl-constricted rabbit aorta were competitively antagonized by CGP 28392. The calcium content of unstimulated tissues was only minimally increased by CGP 28392 but the
45Ca
2+ uptake stimulated by depolarizing levels of K
+ was markedly augmented by this agent. Further analysis of the data indicated that CGP 28392 did not alter the relationship between tension development and
45Ca
2+ uptake. In contrast, CGP 28392 was much less effective in augmenting the contractile response and
45Ca
2+ uptake elicited by noradrenaline. These results thus support the hypothesis that CGP 28392 predominantly facilitates Ca
2+ entry through potential-operated Ca
2+ channels. |
| doi_str_mv | 10.1016/0014-2999(84)90614-9 |
| format | Article |
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45Ca
2+ uptake by vascular smooth muscle were studied using isolated rabbit aorta. CGP 28392 did not elicit contractile responses when administered alone but lowered the threshold for the contractile response to elevated extracellular K
+. CGP 28392 also increased the magnitude of the contractions elicited by submaximal concentrations of K
+. This effect was competitively antagonized by PY 108-068, a Ca antagonist of the dihydropyridine class. Similarly, the relaxing effects of PY 108-068 upon KCl-constricted rabbit aorta were competitively antagonized by CGP 28392. The calcium content of unstimulated tissues was only minimally increased by CGP 28392 but the
45Ca
2+ uptake stimulated by depolarizing levels of K
+ was markedly augmented by this agent. Further analysis of the data indicated that CGP 28392 did not alter the relationship between tension development and
45Ca
2+ uptake. In contrast, CGP 28392 was much less effective in augmenting the contractile response and
45Ca
2+ uptake elicited by noradrenaline. These results thus support the hypothesis that CGP 28392 predominantly facilitates Ca
2+ entry through potential-operated Ca
2+ channels.</description><identifier>ISSN: 0014-2999</identifier><identifier>EISSN: 1879-0712</identifier><identifier>DOI: 10.1016/0014-2999(84)90614-9</identifier><identifier>PMID: 6210203</identifier><identifier>CODEN: EJPHAZ</identifier><language>eng</language><publisher>Amsterdam: Elsevier B.V</publisher><subject>3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester ; Agonist Calcium ; Animals ; aorta ; Biological and medical sciences ; calcium ; Calcium - metabolism ; Calcium Channel Blockers - pharmacology ; Cardiovascular system ; Dihydropyridines ; Dose-Response Relationship, Drug ; Female ; In Vitro Techniques ; Male ; Medical sciences ; Miscellaneous ; Modulation of Ca 2+ entry ; Nifedipine - analogs & derivatives ; Nifedipine - pharmacology ; Pharmacology. Drug treatments ; Potassium Chloride - pharmacology ; Potential operated Ca 2+ channel ; Pyridines - pharmacology ; Rabbit aorta ; Rabbits ; Smooth muscle ; Vasoconstriction - drug effects ; Vasoconstrictor Agents - pharmacology ; vasoconstrictors</subject><ispartof>European journal of pharmacology, 1984-10, Vol.105 (3), p.229-237</ispartof><rights>1984</rights><rights>1985 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c417t-7941b164de4d4d11189a81df77746bf5c07a8325ecb4e19b78ad7063e161dfab3</citedby><cites>FETCH-LOGICAL-c417t-7941b164de4d4d11189a81df77746bf5c07a8325ecb4e19b78ad7063e161dfab3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/0014-2999(84)90614-9$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=9100572$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/6210203$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Loutzenhiser, Rodger</creatorcontrib><creatorcontrib>Rüegg, Urs T.</creatorcontrib><creatorcontrib>Hof, Akiko</creatorcontrib><creatorcontrib>Hof, Robert P.</creatorcontrib><title>Studies on the mechanism of action of the vasoconstrictive dihydropyridine, CGP 28392</title><title>European journal of pharmacology</title><addtitle>Eur J Pharmacol</addtitle><description>The effects of the vasoconstrictive dihydropyridine, CGP 29392, upon tension development and
45Ca
2+ uptake by vascular smooth muscle were studied using isolated rabbit aorta. CGP 28392 did not elicit contractile responses when administered alone but lowered the threshold for the contractile response to elevated extracellular K
+. CGP 28392 also increased the magnitude of the contractions elicited by submaximal concentrations of K
+. This effect was competitively antagonized by PY 108-068, a Ca antagonist of the dihydropyridine class. Similarly, the relaxing effects of PY 108-068 upon KCl-constricted rabbit aorta were competitively antagonized by CGP 28392. The calcium content of unstimulated tissues was only minimally increased by CGP 28392 but the
45Ca
2+ uptake stimulated by depolarizing levels of K
+ was markedly augmented by this agent. Further analysis of the data indicated that CGP 28392 did not alter the relationship between tension development and
45Ca
2+ uptake. In contrast, CGP 28392 was much less effective in augmenting the contractile response and
45Ca
2+ uptake elicited by noradrenaline. These results thus support the hypothesis that CGP 28392 predominantly facilitates Ca
2+ entry through potential-operated Ca
2+ channels.</description><subject>3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester</subject><subject>Agonist Calcium</subject><subject>Animals</subject><subject>aorta</subject><subject>Biological and medical sciences</subject><subject>calcium</subject><subject>Calcium - metabolism</subject><subject>Calcium Channel Blockers - pharmacology</subject><subject>Cardiovascular system</subject><subject>Dihydropyridines</subject><subject>Dose-Response Relationship, Drug</subject><subject>Female</subject><subject>In Vitro Techniques</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Miscellaneous</subject><subject>Modulation of Ca 2+ entry</subject><subject>Nifedipine - analogs & derivatives</subject><subject>Nifedipine - pharmacology</subject><subject>Pharmacology. Drug treatments</subject><subject>Potassium Chloride - pharmacology</subject><subject>Potential operated Ca 2+ channel</subject><subject>Pyridines - pharmacology</subject><subject>Rabbit aorta</subject><subject>Rabbits</subject><subject>Smooth muscle</subject><subject>Vasoconstriction - drug effects</subject><subject>Vasoconstrictor Agents - pharmacology</subject><subject>vasoconstrictors</subject><issn>0014-2999</issn><issn>1879-0712</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1984</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkdFq2zAUhsXoaNNsb7CBL0rZYF51ZNmSbgojdG2h0EHbayFLx0QltjLJCeTtJzchl-uVpPN_50h8IuQL0J9AobmiFHjJlFLfJP-uaJNP6gOZgRSqpALYCZkdkTNyntIrpbRWrD4lpw0Dymg1Iy9P48Z5TEUYinGJRY92aQaf-iJ0hbGjz_W8m6KtScGGIY3R5_oWC-eXOxfDehe98wP-KBa3fwomK8U-kY-dWSX8fFjn5OX3zfPirnx4vL1f_HooLQcxlkJxaKHhDrnjDgCkMhJcJ4TgTdvVlgojK1ajbTmCaoU0TtCmQmgyZdpqTi73c9cx_N1gGnXvk8XVygwYNkmLWrJKSXgXBA6NoIplkO9BG0NKETu9jr43caeB6km7npzqyamWXL9p1yq3fT3M37Q9umPTwXPOLw65SdasumgG69MRU5B_Rky3X-8xzNK2HqNO1uNg0fmIdtQu-P-_4x-t_Jyw</recordid><startdate>19841015</startdate><enddate>19841015</enddate><creator>Loutzenhiser, Rodger</creator><creator>Rüegg, Urs T.</creator><creator>Hof, Akiko</creator><creator>Hof, Robert P.</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>8FD</scope><scope>FR3</scope><scope>M7Z</scope><scope>P64</scope><scope>7X8</scope></search><sort><creationdate>19841015</creationdate><title>Studies on the mechanism of action of the vasoconstrictive dihydropyridine, CGP 28392</title><author>Loutzenhiser, Rodger ; Rüegg, Urs T. ; Hof, Akiko ; Hof, Robert P.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c417t-7941b164de4d4d11189a81df77746bf5c07a8325ecb4e19b78ad7063e161dfab3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1984</creationdate><topic>3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester</topic><topic>Agonist Calcium</topic><topic>Animals</topic><topic>aorta</topic><topic>Biological and medical sciences</topic><topic>calcium</topic><topic>Calcium - metabolism</topic><topic>Calcium Channel Blockers - pharmacology</topic><topic>Cardiovascular system</topic><topic>Dihydropyridines</topic><topic>Dose-Response Relationship, Drug</topic><topic>Female</topic><topic>In Vitro Techniques</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Miscellaneous</topic><topic>Modulation of Ca 2+ entry</topic><topic>Nifedipine - analogs & derivatives</topic><topic>Nifedipine - pharmacology</topic><topic>Pharmacology. Drug treatments</topic><topic>Potassium Chloride - pharmacology</topic><topic>Potential operated Ca 2+ channel</topic><topic>Pyridines - pharmacology</topic><topic>Rabbit aorta</topic><topic>Rabbits</topic><topic>Smooth muscle</topic><topic>Vasoconstriction - drug effects</topic><topic>Vasoconstrictor Agents - pharmacology</topic><topic>vasoconstrictors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Loutzenhiser, Rodger</creatorcontrib><creatorcontrib>Rüegg, Urs T.</creatorcontrib><creatorcontrib>Hof, Akiko</creatorcontrib><creatorcontrib>Hof, Robert P.</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>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biochemistry Abstracts 1</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>European journal of pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Loutzenhiser, Rodger</au><au>Rüegg, Urs T.</au><au>Hof, Akiko</au><au>Hof, Robert P.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Studies on the mechanism of action of the vasoconstrictive dihydropyridine, CGP 28392</atitle><jtitle>European journal of pharmacology</jtitle><addtitle>Eur J Pharmacol</addtitle><date>1984-10-15</date><risdate>1984</risdate><volume>105</volume><issue>3</issue><spage>229</spage><epage>237</epage><pages>229-237</pages><issn>0014-2999</issn><eissn>1879-0712</eissn><coden>EJPHAZ</coden><abstract>The effects of the vasoconstrictive dihydropyridine, CGP 29392, upon tension development and
45Ca
2+ uptake by vascular smooth muscle were studied using isolated rabbit aorta. CGP 28392 did not elicit contractile responses when administered alone but lowered the threshold for the contractile response to elevated extracellular K
+. CGP 28392 also increased the magnitude of the contractions elicited by submaximal concentrations of K
+. This effect was competitively antagonized by PY 108-068, a Ca antagonist of the dihydropyridine class. Similarly, the relaxing effects of PY 108-068 upon KCl-constricted rabbit aorta were competitively antagonized by CGP 28392. The calcium content of unstimulated tissues was only minimally increased by CGP 28392 but the
45Ca
2+ uptake stimulated by depolarizing levels of K
+ was markedly augmented by this agent. Further analysis of the data indicated that CGP 28392 did not alter the relationship between tension development and
45Ca
2+ uptake. In contrast, CGP 28392 was much less effective in augmenting the contractile response and
45Ca
2+ uptake elicited by noradrenaline. These results thus support the hypothesis that CGP 28392 predominantly facilitates Ca
2+ entry through potential-operated Ca
2+ channels.</abstract><cop>Amsterdam</cop><pub>Elsevier B.V</pub><pmid>6210203</pmid><doi>10.1016/0014-2999(84)90614-9</doi><tpages>9</tpages></addata></record> |
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| ispartof | European journal of pharmacology, 1984-10, Vol.105 (3), p.229-237 |
| issn | 0014-2999 1879-0712 |
| language | eng |
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| subjects | 3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester Agonist Calcium Animals aorta Biological and medical sciences calcium Calcium - metabolism Calcium Channel Blockers - pharmacology Cardiovascular system Dihydropyridines Dose-Response Relationship, Drug Female In Vitro Techniques Male Medical sciences Miscellaneous Modulation of Ca 2+ entry Nifedipine - analogs & derivatives Nifedipine - pharmacology Pharmacology. Drug treatments Potassium Chloride - pharmacology Potential operated Ca 2+ channel Pyridines - pharmacology Rabbit aorta Rabbits Smooth muscle Vasoconstriction - drug effects Vasoconstrictor Agents - pharmacology vasoconstrictors |
| title | Studies on the mechanism of action of the vasoconstrictive dihydropyridine, CGP 28392 |
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