L/N-type calcium channel blocker suppresses reflex aldosterone production induced by antihypertensive action
The L/N-type calcium channel blocker cilnidipine has been shown to suppress aldosterone production induced by angiotensin II (Ang II) in vitro. In addition, cilnidipine also suppresses the reflex tachycardia induced by its antihypertensive action in vivo. We investigated the effects of cilnidipine o...
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| Veröffentlicht in: | Heart and vessels 2012-07, Vol.27 (4), p.419-423 |
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| creator | Aritomi, Shizuka Konda, Tomoyuki Yoshimura, Michihiro |
| description | The L/N-type calcium channel blocker cilnidipine has been shown to suppress aldosterone production induced by angiotensin II (Ang II) in vitro. In addition, cilnidipine also suppresses the reflex tachycardia induced by its antihypertensive action in vivo. We investigated the effects of cilnidipine on the reflex aldosterone production induced by its antihypertensive action, to identify the differences in the effects of cilnidipine from those of the L-type calcium channel blocker nifedipine. Male SHR/Izm rats were anesthetized by intraperitoneal injection of pentobarbital sodium, and administered an intravenous infusion of saline supplemented or not with Ang II for 30 min. Blood pressure was monitored continuously in the femoral artery. Each of the calcium channel blockers under study was administered intravenously as a bolus through the femoral vein 1 min after the start of the Ang II infusion, and blood samples were collected 30 min after the start of the Ang II infusion. Following administration at nonhypotensive doses, all calcium channel blockers tended to decrease the plasma aldosterone. In particular, cilnidipine significantly suppressed the plasma aldosterone levels. On the other hand, under the condition of Ang II-induced hypertension, administration of a hypotensive dosage of cilnidipine showed no effect on the plasma aldosterone levels, whereas a hypotensive dosage of nifedipine significantly increased the plasma aldosterone levels. Our results suggest that the L/N-type calcium channel blocker cilnidipine reduces the plasma aldosterone level by suppressing the aldosterone production induced by reflex upregulation of the renin–angiotensin–aldosterone system associated with reduction of the blood pressure. |
| doi_str_mv | 10.1007/s00380-011-0191-8 |
| format | Article |
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In addition, cilnidipine also suppresses the reflex tachycardia induced by its antihypertensive action in vivo. We investigated the effects of cilnidipine on the reflex aldosterone production induced by its antihypertensive action, to identify the differences in the effects of cilnidipine from those of the L-type calcium channel blocker nifedipine. Male SHR/Izm rats were anesthetized by intraperitoneal injection of pentobarbital sodium, and administered an intravenous infusion of saline supplemented or not with Ang II for 30 min. Blood pressure was monitored continuously in the femoral artery. Each of the calcium channel blockers under study was administered intravenously as a bolus through the femoral vein 1 min after the start of the Ang II infusion, and blood samples were collected 30 min after the start of the Ang II infusion. Following administration at nonhypotensive doses, all calcium channel blockers tended to decrease the plasma aldosterone. In particular, cilnidipine significantly suppressed the plasma aldosterone levels. On the other hand, under the condition of Ang II-induced hypertension, administration of a hypotensive dosage of cilnidipine showed no effect on the plasma aldosterone levels, whereas a hypotensive dosage of nifedipine significantly increased the plasma aldosterone levels. Our results suggest that the L/N-type calcium channel blocker cilnidipine reduces the plasma aldosterone level by suppressing the aldosterone production induced by reflex upregulation of the renin–angiotensin–aldosterone system associated with reduction of the blood pressure.</description><identifier>ISSN: 0910-8327</identifier><identifier>EISSN: 1615-2573</identifier><identifier>DOI: 10.1007/s00380-011-0191-8</identifier><identifier>PMID: 21989861</identifier><identifier>CODEN: HEVEEO</identifier><language>eng</language><publisher>Japan: Springer Japan</publisher><subject>ACE inhibitors ; Aldosterone - blood ; Angiotensin II - administration & dosage ; Animals ; Antihypertensive Agents - administration & dosage ; Antihypertensive Agents - pharmacology ; Beta blockers ; Biomedical Engineering and Bioengineering ; Blood Pressure - drug effects ; Calcium ; Calcium Channel Blockers - administration & dosage ; Calcium Channel Blockers - pharmacology ; Calcium Channels, L-Type - drug effects ; Calcium Channels, L-Type - metabolism ; Calcium Channels, N-Type - drug effects ; Calcium Channels, N-Type - metabolism ; Cardiac Surgery ; Cardiology ; Dihydropyridines - administration & dosage ; Dihydropyridines - pharmacology ; Disease Models, Animal ; Down-Regulation ; Hypertension ; Hypertension - blood ; Hypertension - drug therapy ; Hypertension - physiopathology ; Injections, Intravenous ; Male ; Medicine ; Medicine & Public Health ; Nifedipine - pharmacology ; Original Article ; Rats ; Rats, Inbred SHR ; Reflex - drug effects ; Renin-Angiotensin System - drug effects ; Vascular Surgery</subject><ispartof>Heart and vessels, 2012-07, Vol.27 (4), p.419-423</ispartof><rights>Springer 2011</rights><rights>Springer 2012</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-p179t-4f837d7cc28cc60a1eefef0200650428ce3a4e4ef2270bce17ac59e24cdaff843</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00380-011-0191-8$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00380-011-0191-8$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27922,27923,41486,42555,51317</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21989861$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Aritomi, Shizuka</creatorcontrib><creatorcontrib>Konda, Tomoyuki</creatorcontrib><creatorcontrib>Yoshimura, Michihiro</creatorcontrib><title>L/N-type calcium channel blocker suppresses reflex aldosterone production induced by antihypertensive action</title><title>Heart and vessels</title><addtitle>Heart Vessels</addtitle><addtitle>Heart Vessels</addtitle><description>The L/N-type calcium channel blocker cilnidipine has been shown to suppress aldosterone production induced by angiotensin II (Ang II) in vitro. In addition, cilnidipine also suppresses the reflex tachycardia induced by its antihypertensive action in vivo. We investigated the effects of cilnidipine on the reflex aldosterone production induced by its antihypertensive action, to identify the differences in the effects of cilnidipine from those of the L-type calcium channel blocker nifedipine. Male SHR/Izm rats were anesthetized by intraperitoneal injection of pentobarbital sodium, and administered an intravenous infusion of saline supplemented or not with Ang II for 30 min. Blood pressure was monitored continuously in the femoral artery. Each of the calcium channel blockers under study was administered intravenously as a bolus through the femoral vein 1 min after the start of the Ang II infusion, and blood samples were collected 30 min after the start of the Ang II infusion. Following administration at nonhypotensive doses, all calcium channel blockers tended to decrease the plasma aldosterone. In particular, cilnidipine significantly suppressed the plasma aldosterone levels. On the other hand, under the condition of Ang II-induced hypertension, administration of a hypotensive dosage of cilnidipine showed no effect on the plasma aldosterone levels, whereas a hypotensive dosage of nifedipine significantly increased the plasma aldosterone levels. Our results suggest that the L/N-type calcium channel blocker cilnidipine reduces the plasma aldosterone level by suppressing the aldosterone production induced by reflex upregulation of the renin–angiotensin–aldosterone system associated with reduction of the blood pressure.</description><subject>ACE inhibitors</subject><subject>Aldosterone - blood</subject><subject>Angiotensin II - administration & dosage</subject><subject>Animals</subject><subject>Antihypertensive Agents - administration & dosage</subject><subject>Antihypertensive Agents - pharmacology</subject><subject>Beta blockers</subject><subject>Biomedical Engineering and Bioengineering</subject><subject>Blood Pressure - drug effects</subject><subject>Calcium</subject><subject>Calcium Channel Blockers - administration & dosage</subject><subject>Calcium Channel Blockers - pharmacology</subject><subject>Calcium Channels, L-Type - drug effects</subject><subject>Calcium Channels, L-Type - metabolism</subject><subject>Calcium Channels, N-Type - drug effects</subject><subject>Calcium Channels, N-Type - metabolism</subject><subject>Cardiac Surgery</subject><subject>Cardiology</subject><subject>Dihydropyridines - administration & dosage</subject><subject>Dihydropyridines - pharmacology</subject><subject>Disease Models, Animal</subject><subject>Down-Regulation</subject><subject>Hypertension</subject><subject>Hypertension - blood</subject><subject>Hypertension - drug therapy</subject><subject>Hypertension - physiopathology</subject><subject>Injections, Intravenous</subject><subject>Male</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Nifedipine - pharmacology</subject><subject>Original Article</subject><subject>Rats</subject><subject>Rats, Inbred SHR</subject><subject>Reflex - drug effects</subject><subject>Renin-Angiotensin System - drug effects</subject><subject>Vascular Surgery</subject><issn>0910-8327</issn><issn>1615-2573</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNpNkU1LBDEMhosoun78AC9S8DyatPPRHkX8gkUvei7dTsaddbYztjPi_nurq-AhJCQPb0Jexk4RLhCguowAUkEGiCk0ZmqHzbDEIhNFJXfZDDRCpqSoDthhjCsALDTqfXYgUCutSpyxbn75mI2bgbiznWunNXdL6z11fNH17o0Cj9MwBIqRIg_UdPTJbVf3caTQe-JD6OvJjW3veetTRTVfbLj1Y7tMomEkH9sP4vYHOWZ7je0infzmI_Zye_N8fZ_Nn-4erq_m2YCVHrO8UbKqK-eEcq4Ei0QNNSAAygLy1CRpc8qpEaKChSOsrCs0idzVtmlULo_Y-VY3Xfc-URzNqp-CTysN5qWQGguQiTr7pabFmmozhHZtw8b8PScBYgvENPKvFP7JgPl2wGwdMMkB8-2AUfILs2N5Jg</recordid><startdate>20120701</startdate><enddate>20120701</enddate><creator>Aritomi, Shizuka</creator><creator>Konda, Tomoyuki</creator><creator>Yoshimura, Michihiro</creator><general>Springer Japan</general><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>3V.</scope><scope>7QO</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FD</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope></search><sort><creationdate>20120701</creationdate><title>L/N-type calcium channel blocker suppresses reflex aldosterone production induced by antihypertensive action</title><author>Aritomi, Shizuka ; Konda, Tomoyuki ; Yoshimura, Michihiro</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p179t-4f837d7cc28cc60a1eefef0200650428ce3a4e4ef2270bce17ac59e24cdaff843</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>ACE inhibitors</topic><topic>Aldosterone - blood</topic><topic>Angiotensin II - administration & dosage</topic><topic>Animals</topic><topic>Antihypertensive Agents - administration & dosage</topic><topic>Antihypertensive Agents - pharmacology</topic><topic>Beta blockers</topic><topic>Biomedical Engineering and Bioengineering</topic><topic>Blood Pressure - drug effects</topic><topic>Calcium</topic><topic>Calcium Channel Blockers - administration & dosage</topic><topic>Calcium Channel Blockers - pharmacology</topic><topic>Calcium Channels, L-Type - drug effects</topic><topic>Calcium Channels, L-Type - metabolism</topic><topic>Calcium Channels, N-Type - drug effects</topic><topic>Calcium Channels, N-Type - metabolism</topic><topic>Cardiac Surgery</topic><topic>Cardiology</topic><topic>Dihydropyridines - administration & dosage</topic><topic>Dihydropyridines - pharmacology</topic><topic>Disease Models, Animal</topic><topic>Down-Regulation</topic><topic>Hypertension</topic><topic>Hypertension - blood</topic><topic>Hypertension - drug therapy</topic><topic>Hypertension - physiopathology</topic><topic>Injections, Intravenous</topic><topic>Male</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Nifedipine - pharmacology</topic><topic>Original Article</topic><topic>Rats</topic><topic>Rats, Inbred SHR</topic><topic>Reflex - drug effects</topic><topic>Renin-Angiotensin System - drug effects</topic><topic>Vascular Surgery</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Aritomi, Shizuka</creatorcontrib><creatorcontrib>Konda, Tomoyuki</creatorcontrib><creatorcontrib>Yoshimura, Michihiro</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>ProQuest Central (Corporate)</collection><collection>Biotechnology Research Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Research Library (Corporate)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><jtitle>Heart and vessels</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Aritomi, Shizuka</au><au>Konda, Tomoyuki</au><au>Yoshimura, Michihiro</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>L/N-type calcium channel blocker suppresses reflex aldosterone production induced by antihypertensive action</atitle><jtitle>Heart and vessels</jtitle><stitle>Heart Vessels</stitle><addtitle>Heart Vessels</addtitle><date>2012-07-01</date><risdate>2012</risdate><volume>27</volume><issue>4</issue><spage>419</spage><epage>423</epage><pages>419-423</pages><issn>0910-8327</issn><eissn>1615-2573</eissn><coden>HEVEEO</coden><abstract>The L/N-type calcium channel blocker cilnidipine has been shown to suppress aldosterone production induced by angiotensin II (Ang II) in vitro. In addition, cilnidipine also suppresses the reflex tachycardia induced by its antihypertensive action in vivo. We investigated the effects of cilnidipine on the reflex aldosterone production induced by its antihypertensive action, to identify the differences in the effects of cilnidipine from those of the L-type calcium channel blocker nifedipine. Male SHR/Izm rats were anesthetized by intraperitoneal injection of pentobarbital sodium, and administered an intravenous infusion of saline supplemented or not with Ang II for 30 min. Blood pressure was monitored continuously in the femoral artery. Each of the calcium channel blockers under study was administered intravenously as a bolus through the femoral vein 1 min after the start of the Ang II infusion, and blood samples were collected 30 min after the start of the Ang II infusion. Following administration at nonhypotensive doses, all calcium channel blockers tended to decrease the plasma aldosterone. In particular, cilnidipine significantly suppressed the plasma aldosterone levels. On the other hand, under the condition of Ang II-induced hypertension, administration of a hypotensive dosage of cilnidipine showed no effect on the plasma aldosterone levels, whereas a hypotensive dosage of nifedipine significantly increased the plasma aldosterone levels. Our results suggest that the L/N-type calcium channel blocker cilnidipine reduces the plasma aldosterone level by suppressing the aldosterone production induced by reflex upregulation of the renin–angiotensin–aldosterone system associated with reduction of the blood pressure.</abstract><cop>Japan</cop><pub>Springer Japan</pub><pmid>21989861</pmid><doi>10.1007/s00380-011-0191-8</doi><tpages>5</tpages></addata></record> |
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| subjects | ACE inhibitors Aldosterone - blood Angiotensin II - administration & dosage Animals Antihypertensive Agents - administration & dosage Antihypertensive Agents - pharmacology Beta blockers Biomedical Engineering and Bioengineering Blood Pressure - drug effects Calcium Calcium Channel Blockers - administration & dosage Calcium Channel Blockers - pharmacology Calcium Channels, L-Type - drug effects Calcium Channels, L-Type - metabolism Calcium Channels, N-Type - drug effects Calcium Channels, N-Type - metabolism Cardiac Surgery Cardiology Dihydropyridines - administration & dosage Dihydropyridines - pharmacology Disease Models, Animal Down-Regulation Hypertension Hypertension - blood Hypertension - drug therapy Hypertension - physiopathology Injections, Intravenous Male Medicine Medicine & Public Health Nifedipine - pharmacology Original Article Rats Rats, Inbred SHR Reflex - drug effects Renin-Angiotensin System - drug effects Vascular Surgery |
| title | L/N-type calcium channel blocker suppresses reflex aldosterone production induced by antihypertensive action |
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