H. C. Koh, I. C. Shin, J. H. Ha, D. J. Paik, J. S. Kang, C H. Lee
{"title":"cAMP和KATP通道阻断对麻醉大鼠脊髓GABAB受体刺激后心血管反应的影响","authors":"H. C. Koh, I. C. Shin, J. H. Ha, D. J. Paik, J. S. Kang, C H. Lee","doi":"10.1111/j.1365-2680.1999.tb00007.x","DOIUrl":null,"url":null,"abstract":"<div>\n \n <p><b>1</b> Intrathecal (i.t.) injection of baclofen (30, 60 and 100 nmol), a GABA<sub>B</sub> receptor agonist, produced a dose-dependent decrease in blood pressure (BP) and heart rate (HR).</p>\n <p><b>2</b> Pretreatment with 5-aminovaleric acid (50 nmol), a GABA<sub>B</sub> receptor antagonist, blocked the depressor and bradycardic effects of baclofen (100 nmol).</p>\n <p><b>3</b> Pretreatment with 8-bromo-cAMP (10 nmol), a cAMP analogue, attenuated the depressor and bradycardic effects of baclofen (100 nmol), but not with 8-bromo-cGMP (10 nmol), a cGMP analogue.</p>\n <p><b>4</b> In addition, pretreatment with glipizide (20 nmol), an ATP-sensitive K<sup>+</sup> channel (K<sub>ATP</sub>) blocker, attenuated the depressor and bradycardic effects of baclofen (100 nmol).</p>\n <p><b>5</b> These results suggest that GABA<sub>B</sub> receptors in the spinal cord have an inhibitory role in the central cardiovascular regulation and that these depressive and bradycardic actions are modified by cAMP and by K<sub>ATP</sub> channel blockade.</p>\n </div>","PeriodicalId":100151,"journal":{"name":"Autonomic and Autacoid Pharmacology","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2009-01-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1365-2680.1999.tb00007.x","citationCount":"2","resultStr":"{\"title\":\"Modification of cardiovascular responses to spinal GABAB receptor stimulation by cAMP and by KATP channel blockade in anaesthetized rats\",\"authors\":\"H. C. Koh, I. C. Shin, J. H. Ha, D. J. Paik, J. S. Kang, C H. Lee\",\"doi\":\"10.1111/j.1365-2680.1999.tb00007.x\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div>\\n \\n <p><b>1</b> Intrathecal (i.t.) injection of baclofen (30, 60 and 100 nmol), a GABA<sub>B</sub> receptor agonist, produced a dose-dependent decrease in blood pressure (BP) and heart rate (HR).</p>\\n <p><b>2</b> Pretreatment with 5-aminovaleric acid (50 nmol), a GABA<sub>B</sub> receptor antagonist, blocked the depressor and bradycardic effects of baclofen (100 nmol).</p>\\n <p><b>3</b> Pretreatment with 8-bromo-cAMP (10 nmol), a cAMP analogue, attenuated the depressor and bradycardic effects of baclofen (100 nmol), but not with 8-bromo-cGMP (10 nmol), a cGMP analogue.</p>\\n <p><b>4</b> In addition, pretreatment with glipizide (20 nmol), an ATP-sensitive K<sup>+</sup> channel (K<sub>ATP</sub>) blocker, attenuated the depressor and bradycardic effects of baclofen (100 nmol).</p>\\n <p><b>5</b> These results suggest that GABA<sub>B</sub> receptors in the spinal cord have an inhibitory role in the central cardiovascular regulation and that these depressive and bradycardic actions are modified by cAMP and by K<sub>ATP</sub> channel blockade.</p>\\n </div>\",\"PeriodicalId\":100151,\"journal\":{\"name\":\"Autonomic and Autacoid Pharmacology\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2009-01-09\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1111/j.1365-2680.1999.tb00007.x\",\"citationCount\":\"2\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Autonomic and Autacoid Pharmacology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://onlinelibrary.wiley.com/doi/10.1111/j.1365-2680.1999.tb00007.x\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Autonomic and Autacoid Pharmacology","FirstCategoryId":"1085","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1111/j.1365-2680.1999.tb00007.x","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Modification of cardiovascular responses to spinal GABAB receptor stimulation by cAMP and by KATP channel blockade in anaesthetized rats
1 Intrathecal (i.t.) injection of baclofen (30, 60 and 100 nmol), a GABAB receptor agonist, produced a dose-dependent decrease in blood pressure (BP) and heart rate (HR).
2 Pretreatment with 5-aminovaleric acid (50 nmol), a GABAB receptor antagonist, blocked the depressor and bradycardic effects of baclofen (100 nmol).
3 Pretreatment with 8-bromo-cAMP (10 nmol), a cAMP analogue, attenuated the depressor and bradycardic effects of baclofen (100 nmol), but not with 8-bromo-cGMP (10 nmol), a cGMP analogue.
4 In addition, pretreatment with glipizide (20 nmol), an ATP-sensitive K+ channel (KATP) blocker, attenuated the depressor and bradycardic effects of baclofen (100 nmol).
5 These results suggest that GABAB receptors in the spinal cord have an inhibitory role in the central cardiovascular regulation and that these depressive and bradycardic actions are modified by cAMP and by KATP channel blockade.
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