On the top of ARB N/L type Ca channel blocker leads to less elevation of aldosterone
The activation of the renin-angiotensin system (RAS) is one of the unfavourable characteristics of calcium channel blocker (CCB). N type calcium channel is thought to be involved in renin gene transcription and adrenal aldosterone release. Accordingly, N/L type CCB has a possibility of less elevatio...
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| creator | Konoshita, Tadashi Kaeriyama, Saori Urabe, Machi Nakaya, Takahiro Yamada, Mika Ichikawa, Mai Yamamoto, Katsushi Sato, Satsuki Imagawa, Michiko Fujii, Miki Makino, Yasukazu Zenimaru, Yasuo Wakahara, Shigeyuki Suzuki, Jinya Ishizuka, Tamotsu Nakamura, Hiroyuki |
| description | The activation of the renin-angiotensin system (RAS) is one of the unfavourable characteristics of calcium channel blocker (CCB). N type calcium channel is thought to be involved in renin gene transcription and adrenal aldosterone release. Accordingly, N/L type CCB has a possibility of less elevation of plasma aldosterone concentrations (PAC) among CCBs. In a monotherapy study, we had already demonstrated that N/L type CCB leads to less activation of the RAS compared with L type CCB. The objective of this study is to substantiate the hypothesis that at the condition of additive administration on the top of an angiotensin receptor blocker (ARB), still N/L type CCB leads to less elevation of PAC compared with L type one. Subjects were 60 hypertensives administered with valsartan. As an open label study, amlodipine (L type) or cilnidipine (N/L type) were administered on the top of valsartan (ARB) in a cross-over manner. Results were as follows (valsartan+amlodipine compared with valsartan+cilnidipine): systolic blood pressure (SBP)/diastolic blood pressure (DBP) (mmHg): 132±10/76±10 compared with 131±10/77±9, P=0.95/0.48, plasma renin activity (PRA) (ng/ml·h): 2.41±2.67 compared with 2.00±1.50 P=0.20, PAC (pg/ml): 77.3±31.0 compared with 67.4±24.8, P |
| doi_str_mv | 10.1042/BSR20160129 |
| format | Article |
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N type calcium channel is thought to be involved in renin gene transcription and adrenal aldosterone release. Accordingly, N/L type CCB has a possibility of less elevation of plasma aldosterone concentrations (PAC) among CCBs. In a monotherapy study, we had already demonstrated that N/L type CCB leads to less activation of the RAS compared with L type CCB. The objective of this study is to substantiate the hypothesis that at the condition of additive administration on the top of an angiotensin receptor blocker (ARB), still N/L type CCB leads to less elevation of PAC compared with L type one. Subjects were 60 hypertensives administered with valsartan. As an open label study, amlodipine (L type) or cilnidipine (N/L type) were administered on the top of valsartan (ARB) in a cross-over manner. Results were as follows (valsartan+amlodipine compared with valsartan+cilnidipine): systolic blood pressure (SBP)/diastolic blood pressure (DBP) (mmHg): 132±10/76±10 compared with 131±10/77±9, P=0.95/0.48, plasma renin activity (PRA) (ng/ml·h): 2.41±2.67 compared with 2.00±1.50 P=0.20, PAC (pg/ml): 77.3±31.0 compared with 67.4±24.8, P<0.05, urinary albumin excretion (UAE) (mg/gCr): 105.9±216.1 compared with 73.9±122.2, P<0.05. Thus, PAC at cilnidipine was significantly lower than those at amlodipine in spite of the comparable BP reductions. Besides, UAE was significantly lower at cilnidipine. In conclusion, on the top of the ARB, it is suggested that cilnidipine administration might lead to less elevation of PAC and reduction in UAE compared with amlodipine.</description><identifier>ISSN: 0144-8463</identifier><identifier>EISSN: 1573-4935</identifier><identifier>DOI: 10.1042/BSR20160129</identifier><identifier>PMID: 27515419</identifier><language>eng</language><publisher>England: Portland Press Ltd</publisher><subject>Aged ; Aldosterone - blood ; Amlodipine - administration & dosage ; Angiotensin Receptor Antagonists - administration & dosage ; Blood Pressure - drug effects ; Calcium Channel Blockers - administration & dosage ; Calcium Channels, L-Type - drug effects ; Calcium Channels, L-Type - genetics ; Calcium Channels, N-Type - drug effects ; Calcium Channels, N-Type - genetics ; Dihydropyridines - administration & dosage ; Drug Combinations ; Female ; Humans ; Hypertension - blood ; Hypertension - drug therapy ; Hypertension - pathology ; Male ; Middle Aged ; Original Paper ; Original Papers ; Renin-Angiotensin System - drug effects ; Valsartan - administration & dosage</subject><ispartof>Bioscience reports, 2016-10, Vol.36 (5)</ispartof><rights>2016 The Author(s).</rights><rights>2016 The Author(s) 2016</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c517t-77fd17bf61a462c791e40e83bedf492ff0d4d8f5b8b810f6e9e9f3b483bd99263</citedby><cites>FETCH-LOGICAL-c517t-77fd17bf61a462c791e40e83bedf492ff0d4d8f5b8b810f6e9e9f3b483bd99263</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5025805/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5025805/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27515419$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Konoshita, Tadashi</creatorcontrib><creatorcontrib>Kaeriyama, Saori</creatorcontrib><creatorcontrib>Urabe, Machi</creatorcontrib><creatorcontrib>Nakaya, Takahiro</creatorcontrib><creatorcontrib>Yamada, Mika</creatorcontrib><creatorcontrib>Ichikawa, Mai</creatorcontrib><creatorcontrib>Yamamoto, Katsushi</creatorcontrib><creatorcontrib>Sato, Satsuki</creatorcontrib><creatorcontrib>Imagawa, Michiko</creatorcontrib><creatorcontrib>Fujii, Miki</creatorcontrib><creatorcontrib>Makino, Yasukazu</creatorcontrib><creatorcontrib>Zenimaru, Yasuo</creatorcontrib><creatorcontrib>Wakahara, Shigeyuki</creatorcontrib><creatorcontrib>Suzuki, Jinya</creatorcontrib><creatorcontrib>Ishizuka, Tamotsu</creatorcontrib><creatorcontrib>Nakamura, Hiroyuki</creatorcontrib><creatorcontrib>Genomic Disease Outcome Consortium (G-DOC) Study Investigators</creatorcontrib><creatorcontrib>for the Genomic Disease Outcome Consortium (G-DOC) Study Investigators</creatorcontrib><title>On the top of ARB N/L type Ca channel blocker leads to less elevation of aldosterone</title><title>Bioscience reports</title><addtitle>Biosci Rep</addtitle><description>The activation of the renin-angiotensin system (RAS) is one of the unfavourable characteristics of calcium channel blocker (CCB). N type calcium channel is thought to be involved in renin gene transcription and adrenal aldosterone release. Accordingly, N/L type CCB has a possibility of less elevation of plasma aldosterone concentrations (PAC) among CCBs. In a monotherapy study, we had already demonstrated that N/L type CCB leads to less activation of the RAS compared with L type CCB. The objective of this study is to substantiate the hypothesis that at the condition of additive administration on the top of an angiotensin receptor blocker (ARB), still N/L type CCB leads to less elevation of PAC compared with L type one. Subjects were 60 hypertensives administered with valsartan. As an open label study, amlodipine (L type) or cilnidipine (N/L type) were administered on the top of valsartan (ARB) in a cross-over manner. Results were as follows (valsartan+amlodipine compared with valsartan+cilnidipine): systolic blood pressure (SBP)/diastolic blood pressure (DBP) (mmHg): 132±10/76±10 compared with 131±10/77±9, P=0.95/0.48, plasma renin activity (PRA) (ng/ml·h): 2.41±2.67 compared with 2.00±1.50 P=0.20, PAC (pg/ml): 77.3±31.0 compared with 67.4±24.8, P<0.05, urinary albumin excretion (UAE) (mg/gCr): 105.9±216.1 compared with 73.9±122.2, P<0.05. Thus, PAC at cilnidipine was significantly lower than those at amlodipine in spite of the comparable BP reductions. Besides, UAE was significantly lower at cilnidipine. In conclusion, on the top of the ARB, it is suggested that cilnidipine administration might lead to less elevation of PAC and reduction in UAE compared with amlodipine.</description><subject>Aged</subject><subject>Aldosterone - blood</subject><subject>Amlodipine - administration & dosage</subject><subject>Angiotensin Receptor Antagonists - administration & dosage</subject><subject>Blood Pressure - drug effects</subject><subject>Calcium Channel Blockers - administration & dosage</subject><subject>Calcium Channels, L-Type - drug effects</subject><subject>Calcium Channels, L-Type - genetics</subject><subject>Calcium Channels, N-Type - drug effects</subject><subject>Calcium Channels, N-Type - genetics</subject><subject>Dihydropyridines - administration & dosage</subject><subject>Drug Combinations</subject><subject>Female</subject><subject>Humans</subject><subject>Hypertension - blood</subject><subject>Hypertension - drug therapy</subject><subject>Hypertension - pathology</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Original Paper</subject><subject>Original Papers</subject><subject>Renin-Angiotensin System - drug effects</subject><subject>Valsartan - administration & dosage</subject><issn>0144-8463</issn><issn>1573-4935</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkctOwzAQRS0EglJYsUdeIqFQj2Mn8QaprXhJFZV4rC0nGdOAG4c4ReJv-Ba-jFQ8VFYz0j1zZzSXkCNgZ8AEH03u7ziDhAFXW2QAMo0joWK5TQYMhIgykcR7ZD-EZ8ZYL4hdssdTCVKAGpDHeU27BdLON9RbOr6b0NvRjHbvDX5-TA0tFqau0dHc-eIFW-rQlKGn-yYEig7fTFf5ej1rXOlDh62v8YDsWOMCHv7UIXm8vHiYXkez-dXNdDyLCglpF6WpLSHNbQJGJLxIFaBgmMU5llYobi0rRZlZmWd5BswmqFDZOBc9USrFk3hIzr99m1W-xLLAumuN001bLU37rr2p9H-lrhb6yb9pybjMmOwNTn4MWv-6wtDpZRUKdM7U6FdBQ8aZVAJS6NHTb7RofQgt2r81wPQ6CL0RRE8fb172x_5-Pv4C84uEHQ</recordid><startdate>20161001</startdate><enddate>20161001</enddate><creator>Konoshita, Tadashi</creator><creator>Kaeriyama, Saori</creator><creator>Urabe, Machi</creator><creator>Nakaya, Takahiro</creator><creator>Yamada, Mika</creator><creator>Ichikawa, Mai</creator><creator>Yamamoto, Katsushi</creator><creator>Sato, Satsuki</creator><creator>Imagawa, Michiko</creator><creator>Fujii, Miki</creator><creator>Makino, Yasukazu</creator><creator>Zenimaru, Yasuo</creator><creator>Wakahara, Shigeyuki</creator><creator>Suzuki, Jinya</creator><creator>Ishizuka, Tamotsu</creator><creator>Nakamura, Hiroyuki</creator><general>Portland Press Ltd</general><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><scope>5PM</scope></search><sort><creationdate>20161001</creationdate><title>On the top of ARB N/L type Ca channel blocker leads to less elevation of aldosterone</title><author>Konoshita, Tadashi ; Kaeriyama, Saori ; Urabe, Machi ; Nakaya, Takahiro ; Yamada, Mika ; Ichikawa, Mai ; Yamamoto, Katsushi ; Sato, Satsuki ; Imagawa, Michiko ; Fujii, Miki ; Makino, Yasukazu ; Zenimaru, Yasuo ; Wakahara, Shigeyuki ; Suzuki, Jinya ; Ishizuka, Tamotsu ; Nakamura, Hiroyuki</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c517t-77fd17bf61a462c791e40e83bedf492ff0d4d8f5b8b810f6e9e9f3b483bd99263</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Aged</topic><topic>Aldosterone - blood</topic><topic>Amlodipine - administration & dosage</topic><topic>Angiotensin Receptor Antagonists - administration & dosage</topic><topic>Blood Pressure - drug effects</topic><topic>Calcium Channel Blockers - administration & dosage</topic><topic>Calcium Channels, L-Type - drug effects</topic><topic>Calcium Channels, L-Type - genetics</topic><topic>Calcium Channels, N-Type - drug effects</topic><topic>Calcium Channels, N-Type - genetics</topic><topic>Dihydropyridines - administration & dosage</topic><topic>Drug Combinations</topic><topic>Female</topic><topic>Humans</topic><topic>Hypertension - blood</topic><topic>Hypertension - drug therapy</topic><topic>Hypertension - pathology</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Original Paper</topic><topic>Original Papers</topic><topic>Renin-Angiotensin System - drug effects</topic><topic>Valsartan - administration & dosage</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Konoshita, Tadashi</creatorcontrib><creatorcontrib>Kaeriyama, Saori</creatorcontrib><creatorcontrib>Urabe, Machi</creatorcontrib><creatorcontrib>Nakaya, Takahiro</creatorcontrib><creatorcontrib>Yamada, Mika</creatorcontrib><creatorcontrib>Ichikawa, Mai</creatorcontrib><creatorcontrib>Yamamoto, Katsushi</creatorcontrib><creatorcontrib>Sato, Satsuki</creatorcontrib><creatorcontrib>Imagawa, Michiko</creatorcontrib><creatorcontrib>Fujii, Miki</creatorcontrib><creatorcontrib>Makino, Yasukazu</creatorcontrib><creatorcontrib>Zenimaru, Yasuo</creatorcontrib><creatorcontrib>Wakahara, Shigeyuki</creatorcontrib><creatorcontrib>Suzuki, Jinya</creatorcontrib><creatorcontrib>Ishizuka, Tamotsu</creatorcontrib><creatorcontrib>Nakamura, Hiroyuki</creatorcontrib><creatorcontrib>Genomic Disease Outcome Consortium (G-DOC) Study Investigators</creatorcontrib><creatorcontrib>for the Genomic Disease Outcome Consortium (G-DOC) Study Investigators</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><collection>PubMed Central (Full Participant titles)</collection><jtitle>Bioscience reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Konoshita, Tadashi</au><au>Kaeriyama, Saori</au><au>Urabe, Machi</au><au>Nakaya, Takahiro</au><au>Yamada, Mika</au><au>Ichikawa, Mai</au><au>Yamamoto, Katsushi</au><au>Sato, Satsuki</au><au>Imagawa, Michiko</au><au>Fujii, Miki</au><au>Makino, Yasukazu</au><au>Zenimaru, Yasuo</au><au>Wakahara, Shigeyuki</au><au>Suzuki, Jinya</au><au>Ishizuka, Tamotsu</au><au>Nakamura, Hiroyuki</au><aucorp>Genomic Disease Outcome Consortium (G-DOC) Study Investigators</aucorp><aucorp>for the Genomic Disease Outcome Consortium (G-DOC) Study Investigators</aucorp><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>On the top of ARB N/L type Ca channel blocker leads to less elevation of aldosterone</atitle><jtitle>Bioscience reports</jtitle><addtitle>Biosci Rep</addtitle><date>2016-10-01</date><risdate>2016</risdate><volume>36</volume><issue>5</issue><issn>0144-8463</issn><eissn>1573-4935</eissn><abstract>The activation of the renin-angiotensin system (RAS) is one of the unfavourable characteristics of calcium channel blocker (CCB). N type calcium channel is thought to be involved in renin gene transcription and adrenal aldosterone release. Accordingly, N/L type CCB has a possibility of less elevation of plasma aldosterone concentrations (PAC) among CCBs. In a monotherapy study, we had already demonstrated that N/L type CCB leads to less activation of the RAS compared with L type CCB. The objective of this study is to substantiate the hypothesis that at the condition of additive administration on the top of an angiotensin receptor blocker (ARB), still N/L type CCB leads to less elevation of PAC compared with L type one. Subjects were 60 hypertensives administered with valsartan. As an open label study, amlodipine (L type) or cilnidipine (N/L type) were administered on the top of valsartan (ARB) in a cross-over manner. Results were as follows (valsartan+amlodipine compared with valsartan+cilnidipine): systolic blood pressure (SBP)/diastolic blood pressure (DBP) (mmHg): 132±10/76±10 compared with 131±10/77±9, P=0.95/0.48, plasma renin activity (PRA) (ng/ml·h): 2.41±2.67 compared with 2.00±1.50 P=0.20, PAC (pg/ml): 77.3±31.0 compared with 67.4±24.8, P<0.05, urinary albumin excretion (UAE) (mg/gCr): 105.9±216.1 compared with 73.9±122.2, P<0.05. Thus, PAC at cilnidipine was significantly lower than those at amlodipine in spite of the comparable BP reductions. Besides, UAE was significantly lower at cilnidipine. In conclusion, on the top of the ARB, it is suggested that cilnidipine administration might lead to less elevation of PAC and reduction in UAE compared with amlodipine.</abstract><cop>England</cop><pub>Portland Press Ltd</pub><pmid>27515419</pmid><doi>10.1042/BSR20160129</doi><oa>free_for_read</oa></addata></record> |
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| subjects | Aged Aldosterone - blood Amlodipine - administration & dosage Angiotensin Receptor Antagonists - administration & dosage Blood Pressure - drug effects Calcium Channel Blockers - administration & dosage Calcium Channels, L-Type - drug effects Calcium Channels, L-Type - genetics Calcium Channels, N-Type - drug effects Calcium Channels, N-Type - genetics Dihydropyridines - administration & dosage Drug Combinations Female Humans Hypertension - blood Hypertension - drug therapy Hypertension - pathology Male Middle Aged Original Paper Original Papers Renin-Angiotensin System - drug effects Valsartan - administration & dosage |
| title | On the top of ARB N/L type Ca channel blocker leads to less elevation of aldosterone |
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