title: On the top of ARB N/L type Ca channel blocker leads to less elevation of aldosterone.
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.
authors: Third Department of Internal Medicine, University of Fukui Faculty of Medical Sciences, Fukui, Japan konosita@u-fukui.ac.jp.
authors: Tadashi
authors: T
authors: Konoshita
authors: Third Department of Internal Medicine, University of Fukui Faculty of Medical Sciences, Fukui, Japan.
authors: Saori
authors: S
authors: Kaeriyama
authors: Third Department of Internal Medicine, University of Fukui Faculty of Medical Sciences, Fukui, Japan.
authors: Machi
authors: M
authors: Urabe
authors: Third Department of Internal Medicine, University of Fukui Faculty of Medical Sciences, Fukui, Japan.
authors: Takahiro
authors: T
authors: Nakaya
authors: Third Department of Internal Medicine, University of Fukui Faculty of Medical Sciences, Fukui, Japan.
authors: Mika
authors: M
authors: Yamada
authors: Third Department of Internal Medicine, University of Fukui Faculty of Medical Sciences, Fukui, Japan.
authors: Mai
authors: M
authors: Ichikawa
authors: Third Department of Internal Medicine, University of Fukui Faculty of Medical Sciences, Fukui, Japan.
authors: Katsushi
authors: K
authors: Yamamoto
authors: Third Department of Internal Medicine, University of Fukui Faculty of Medical Sciences, Fukui, Japan.
authors: Satsuki
authors: S
authors: Sato
authors: Third Department of Internal Medicine, University of Fukui Faculty of Medical Sciences, Fukui, Japan.
authors: Michiko
authors: M
authors: Imagawa
authors: Third Department of Internal Medicine, University of Fukui Faculty of Medical Sciences, Fukui, Japan.
authors: Miki
authors: M
authors: Fujii
authors: Third Department of Internal Medicine, University of Fukui Faculty of Medical Sciences, Fukui, Japan.
authors: Yasukazu
authors: Y
authors: Makino
authors: Third Department of Internal Medicine, University of Fukui Faculty of Medical Sciences, Fukui, Japan.
authors: Yasuo
authors: Y
authors: Zenimaru
authors: Third Department of Internal Medicine, University of Fukui Faculty of Medical Sciences, Fukui, Japan.
authors: Shigeyuki
authors: S
authors: Wakahara
authors: Third Department of Internal Medicine, University of Fukui Faculty of Medical Sciences, Fukui, Japan.
authors: Jinya
authors: J
authors: Suzuki
authors: Third Department of Internal Medicine, University of Fukui Faculty of Medical Sciences, Fukui, Japan.
authors: Tamotsu
authors: T
authors: Ishizuka
authors: Department of Environmental and Preventive Medicine, Kanazawa University Graduate School of Medical Science, Kanazawa, Japan.
authors: Hiroyuki
authors: H
authors: Nakamura
mesh_terms: D000368:Aged; D000450:Aldosterone / Q000097:blood*; D017311:Amlodipine / Q000008:administration & dosage; D057911:Angiotensin Receptor Antagonists / Q000008:administration & dosage*; D001794:Blood Pressure / Q000187:drug effects; D002121:Calcium Channel Blockers / Q000008:administration & dosage*; D020746:Calcium Channels, L-Type / Q000187:drug effects / Q000235:genetics; D020864:Calcium Channels, N-Type / Q000187:drug effects / Q000235:genetics; D004095:Dihydropyridines / Q000008:administration & dosage; D004338:Drug Combinations; D005260:Female; D006801:Humans; D006973:Hypertension / Q000097:blood / Q000188:drug therapy* / Q000473:pathology; D008297:Male; D008875:Middle Aged; D012084:Renin-Angiotensin System / Q000187:drug effects; D000068756:Valsartan / Q000008:administration & dosage
chemical_list: D057911:Angiotensin Receptor Antagonists; D002121:Calcium Channel Blockers; D020746:Calcium Channels, L-Type; D020864:Calcium Channels, N-Type; D004095:Dihydropyridines; D004338:Drug Combinations; D017311:Amlodipine; D000450:Aldosterone; D000068756:Valsartan; C065927:cilnidipine
keywords: aldosterone; amlodipine; angiotensin receptor blocker; calcium channel blocker; cilnidipine; renin; renin–angiotensin system