title: Effects of amlodipine and cilnidipine on cardiac sympathetic nervous system and neurohormonal status in essential hypertension.
abstract: N-Type calcium channel antagonists may suppress sympathetic activity. The purpose of this study was to assess the effects of amlodipine and cilnidipine on the cardiac sympathetic nervous system and the neurohormonal status of essential hypertension. 123I-metaiodobenzylguanidine (MIBG) cardiac imaging was performed and blood samples were taken to determine plasma renin activity and plasma norepinephrine concentration before and 3 months after drug administration in 47 patients with mild essential hypertension. Twenty-four of the patients were treated with 5 to 10 mg/d of amlodipine; the other 23 were treated with 10 to 20 mg/d of cilnidipine. For comparison, 12 normotensive subjects were also studied. No significant differences were found in the basal characteristics between the 2 hypertensive groups. In both hypertensive groups, both the systolic and diastolic blood pressures were significantly reduced to similar levels 3 months after drug treatment. Before the drug treatment, the 2 hypertensive groups had a significantly higher washout rate and lower heart-to-mediastinum (H/M) ratio compared with the normotensive subjects. The H/M ratio significantly increased (P<0.05) in combination with a decreased washout rate (P<0.02) after drug treatment in the cilnidipine group. In the amlodipine group, a significant decrease in washout rate (P<0. 04) was noted, without an increase in the H/M ratio. However, no significant changes were found in plasma renin activity and plasma norepinephrine concentration in either group. Thus, in patients with essential hypertension, cilnidipine suppressed cardiac sympathetic overactivity and amlodipine had a little suppressive effect. Cilnidipine may provide a new strategy for treatment of cardiovascular diseases with sympathetic overactivity.
authors.affiliation: Department of Cardiology, Shizuoka General Hospital, Shizuoka, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Sakata
authors.forename: M
authors.initials: M
authors.lastname: Shirotani
authors.forename: H
authors.initials: H
authors.lastname: Yoshida
authors.forename: R
authors.initials: R
authors.lastname: Nawada
authors.forename: K
authors.initials: K
authors.lastname: Obayashi
authors.forename: K
authors.initials: K
authors.lastname: Togi
authors.forename: N
authors.initials: N
authors.lastname: Miho
mesh_terms: D000328:Adult; D000368:Aged; D017311:Amlodipine / Q000494:pharmacology / Q000627:therapeutic use*; D001794:Blood Pressure / Q000187:drug effects; D002121:Calcium Channel Blockers / Q000494:pharmacology / Q000627:therapeutic use*; D004095:Dihydropyridines / Q000494:pharmacology / Q000627:therapeutic use*; D005260:Female; D006321:Heart / Q000294:innervation*; D006339:Heart Rate / Q000187:drug effects; D006439:Hemodynamics / Q000187:drug effects* / Q000502:physiology; D006801:Humans; D006973:Hypertension / Q000097:blood / Q000188:drug therapy* / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D009638:Norepinephrine / Q000097:blood; D012016:Reference Values; D012083:Renin / Q000097:blood; D013564:Sympathetic Nervous System / Q000187:drug effects* / Q000502:physiology / Q000503:physiopathology
chemical_list: D002121:Calcium Channel Blockers; D004095:Dihydropyridines; D017311:Amlodipine; C065927:cilnidipine; D012083:Renin; D009638:Norepinephrine