{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,7,30]],"date-time":"2025-07-30T10:37:12Z","timestamp":1753871832229,"version":"3.41.2"},"reference-count":39,"publisher":"Portland Press Ltd.","issue":"5","license":[{"start":{"date-parts":[[2019,7,25]],"date-time":"2019-07-25T00:00:00Z","timestamp":1564012800000},"content-version":"vor","delay-in-days":1042,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["portlandpress.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2016,10,1]]},"abstract":"<jats:p>The activation of the renin\u2013angiotensin system (RAS) is one of the unfavourable characteristics of calcium channel blocker (CCB). N type\u00a0calcium channel is thought to be involved in renin gene transcription and adrenal aldosterone release. Accordingly, N\/L type\u00a0CCB 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\u00a0CCB leads to less activation of the RAS compared with L type\u00a0CCB. 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\u00a0CCB leads to less elevation of PAC compared with L type\u00a0one. 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\u00b110\/76\u00b110 compared with 131\u00b110\/77\u00b19, P=0.95\/0.48, plasma renin activity (PRA) (ng\/ml\u00b7h): 2.41\u00b12.67 compared with 2.00\u00b11.50 P=0.20, PAC (pg\/ml): 77.3\u00b131.0 compared with 67.4\u00b124.8, P&amp;lt;0.05, urinary albumin excretion (UAE) (mg\/gCr): 105.9\u00b1216.1 compared with 73.9\u00b1122.2, P&amp;lt;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.<\/jats:p>","DOI":"10.1042\/bsr20160129","type":"journal-article","created":{"date-parts":[[2016,8,12]],"date-time":"2016-08-12T02:09:17Z","timestamp":1470967757000},"update-policy":"https:\/\/doi.org\/10.1042\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["On the top of ARB N\/L type\u00a0Ca channel blocker leads to less elevation of aldosterone"],"prefix":"10.1042","volume":"36","author":[{"given":"Tadashi","family":"Konoshita","sequence":"first","affiliation":[{"name":"Third Department of Internal Medicine, University of Fukui Faculty of Medical Sciences, Fukui, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Saori","family":"Kaeriyama","sequence":"additional","affiliation":[{"name":"Third Department of Internal Medicine, University of Fukui Faculty of Medical Sciences, Fukui, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Machi","family":"Urabe","sequence":"additional","affiliation":[{"name":"Third Department of Internal Medicine, University of Fukui Faculty of Medical Sciences, Fukui, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Takahiro","family":"Nakaya","sequence":"additional","affiliation":[{"name":"Third Department of Internal Medicine, University of Fukui Faculty of Medical Sciences, Fukui, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Mika","family":"Yamada","sequence":"additional","affiliation":[{"name":"Third Department of Internal Medicine, University of Fukui Faculty of Medical Sciences, Fukui, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Mai","family":"Ichikawa","sequence":"additional","affiliation":[{"name":"Third Department of Internal Medicine, University of Fukui Faculty of Medical Sciences, Fukui, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Katsushi","family":"Yamamoto","sequence":"additional","affiliation":[{"name":"Third Department of Internal Medicine, University of Fukui Faculty of Medical Sciences, Fukui, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Satsuki","family":"Sato","sequence":"additional","affiliation":[{"name":"Third Department of Internal Medicine, University of Fukui Faculty of Medical Sciences, Fukui, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Michiko","family":"Imagawa","sequence":"additional","affiliation":[{"name":"Third Department of Internal Medicine, University of Fukui Faculty of Medical Sciences, Fukui, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Miki","family":"Fujii","sequence":"additional","affiliation":[{"name":"Third Department of Internal Medicine, University of Fukui Faculty of Medical Sciences, Fukui, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yasukazu","family":"Makino","sequence":"additional","affiliation":[{"name":"Third Department of Internal Medicine, University of Fukui Faculty of Medical Sciences, Fukui, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yasuo","family":"Zenimaru","sequence":"additional","affiliation":[{"name":"Third Department of Internal Medicine, University of Fukui Faculty of Medical Sciences, Fukui, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Shigeyuki","family":"Wakahara","sequence":"additional","affiliation":[{"name":"Third Department of Internal Medicine, University of Fukui Faculty of Medical Sciences, Fukui, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jinya","family":"Suzuki","sequence":"additional","affiliation":[{"name":"Third Department of Internal Medicine, University of Fukui Faculty of Medical Sciences, Fukui, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Tamotsu","family":"Ishizuka","sequence":"additional","affiliation":[{"name":"Third Department of Internal Medicine, University of Fukui Faculty of Medical Sciences, Fukui, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hiroyuki","family":"Nakamura","sequence":"additional","affiliation":[{"name":"Department of Environmental and Preventive Medicine, Kanazawa University Graduate School of Medical Science, Kanazawa, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"name":"for the Genomic Disease Outcome Consortium (G-DOC) Study Investigators","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"288","published-online":{"date-parts":[[2016,9,16]]},"reference":[{"key":"2021111619155199800_B1","first-page":"229","article-title":"Molecular genetics of the renin-angiotensin-aldosterone system in human hypertension","volume":"45","author":"Corvol","year":"1997","journal-title":"Pathol. 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