title: Effects of long-acting calcium channel antagonists on neurohumoral factors: comparison of nifedipine coat-core with amlodipine.
abstract: Calcium channel antagonists can induce sympathetic hyperactivity, leading to a poor prognosis for hypertensive patients. Nifedipine formulations that allow once-daily administration are now available for use in clinical practice. To compare the effects of nifedipine with those of amlodipine, we studied 36 essential hypertensive patients. Those who had been administered nifedipine sustained-release were treated with amlodipine in place of nifedipine sustained-release, and those who had been administered amlodipine were treated with nifedipine coat-core in place of amlodipine. Substitution of nifedipine sustained-release by amlodipine had no significant effect on hypertensive symptoms. However, the plasma levels of norepinephrine, renin, and aldosterone were significantly lower (p < 0.001-0.05) in patients taking amlodipine in place of nifedipine sustained-release. Substitution of amlodipine by nifedipine coat-core again had no significant effect on hypertensive symptoms. However, the plasma levels of norepinephrine, renin, and aldosterone did not change significantly after the substitution. These findings indicate that, at the effective anti-hypertensive concentrations of nifedipine coat-core and amlodipine, nifedipine coat-core may not increase sympathetic nerve activity as is observed with amlodipine. The results also suggest that the duration of action of nifedipine formulations is an important determinant for nifedipine-induced hyperactivity in the reflex sympathetic nerve and the renin-angiotensin systems.
authors.affiliation: First Department of Internal Medicine, Shiga University of Medical Science, Seta, Otsu, Japan. tutamoto@belle.shiga-med.ac.jp
authors.forename: Takayoshi
authors.initials: T
authors.lastname: Tsutamoto
authors.forename: Takashi
authors.initials: T
authors.lastname: Tsutsui
authors.forename: Keiko
authors.initials: K
authors.lastname: Maeda
authors.forename: Masaru
authors.initials: M
authors.lastname: Hayashi
authors.forename: Atsuyuki
authors.initials: A
authors.lastname: Wada
authors.forename: Masato
authors.initials: M
authors.lastname: Ohnishi
authors.forename: Masanori
authors.initials: M
authors.lastname: Fujii
authors.forename: Chitose
authors.initials: C
authors.lastname: Ishii
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D000450:Aldosterone / Q000097:blood*; D017311:Amlodipine / Q000494:pharmacology / Q000627:therapeutic use; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D002121:Calcium Channel Blockers / Q000494:pharmacology* / Q000627:therapeutic use; D002626:Chemistry, Pharmaceutical; D016009:Chi-Square Distribution; D003692:Delayed-Action Preparations; D005260:Female; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology; D006801:Humans; D006973:Hypertension / Q000097:blood / Q000188:drug therapy; D008297:Male; D008875:Middle Aged; D018377:Neurotransmitter Agents / Q000097:blood; D009543:Nifedipine / Q000494:pharmacology* / Q000627:therapeutic use; D009638:Norepinephrine / Q000097:blood*; D012083:Renin / Q000097:blood*
chemical_list: D002121:Calcium Channel Blockers; D003692:Delayed-Action Preparations; D018377:Neurotransmitter Agents; D017311:Amlodipine; D000450:Aldosterone; D012083:Renin; D009543:Nifedipine; D009638:Norepinephrine