Comparison of the anti-hypertensive effects of the L/N-type calcium channel antagonist cilnidipine, and the L-type calcium channel antagonist amlodipine in hypertensive patients with cerebrovascular disease.
OBJECTIVE
It is known that the risk of cerebral stroke recurrence in post-stroke patients is comparatively higher than in normal subjects, and it is suggested that autonomic nervous system dysfunctions elevate this risk. We investigated the anti-hypertensive effects of cilnidipine, a Ca antagonist which suppresses sympathetic nerve activation, in hypertensives with chronic-stage cerebrovascular disease in a comparison with amlodipine.


METHODS
Amlodipine 5-7.5 mg/day, or cilnidipine 5-10 mg/day was administered to 78 hypertensive subjects (greater than 140 mmHg systolic, or 90 mmHg diastolic) undergoing outpatient treatment. Amlodipine or cilnidipine was also administered similarly, to 30 subjects having hypertension associated with a cerebral infarct which occurred more than one month earlier due to cerebral thrombosis or embolism. After 3 months administration, the subjects' blood pressures and pulse rates were recorded with an ambulatory blood pressure monitor over 24 hours.


RESULTS
No difference was recognized in patient age, gender, and systolic and diastolic blood pressure before treatment between the groups. In the cilnidipine groups, no difference in average 24-hour or waking systolic blood pressure values was seen between cerebrovascular disease (CVD) subjects and non-CVD subjects, although in the amlodipine groups, CVD subjects had significantly higher blood pressure values than non-CVD subjects. In the cilnidipine group, the coefficient of variation values of pulse rate were significantly higher in CVD subjects than in non-CVD subjects (p<0.05).


CONCLUSIONS
In patients with recent stroke, a Ca antagonist with no sympathetic nerve suppression had weaker blood pressure-lowering effects. Significantly increased pulse rate variability, shown in the CVD subjects administered cilnidipine, suggests that cilnidipine enhanced the parasympathetic function in hypertensive patients with CVD.
Takei
Kazuo
K
Department of Neurology, School of Medicine, Saitama Medical University.
Araki
Nobuo
N
Ohkubo
Takeshi
T
Tamura
Naotoshi
N
Yamamoto
Toshimasa
T
Furuya
Daisuke
D
Yanagisawa
Chiaki Takano
CT
Shimazu
Kunio
K
D000368:Aged; D017311:Amlodipine / Q000494:pharmacology / Q000627:therapeutic use*; D000959:Antihypertensive Agents / Q000494:pharmacology / Q000627:therapeutic use*; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D002121:Calcium Channel Blockers / Q000494:pharmacology / Q000627:therapeutic use*; D020746:Calcium Channels, L-Type / Q000378:metabolism; D020864:Calcium Channels, N-Type / Q000378:metabolism; D002561:Cerebrovascular Disorders / Q000150:complications / Q000188:drug therapy* / Q000378:metabolism; D004095:Dihydropyridines / Q000494:pharmacology / Q000627:therapeutic use*; D005260:Female; D006801:Humans; D006973:Hypertension / Q000150:complications / Q000188:drug therapy* / Q000378:metabolism; D008297:Male; D008875:Middle Aged
D000959:Antihypertensive Agents; D002121:Calcium Channel Blockers; D020746:Calcium Channels, L-Type; D020864:Calcium Channels, N-Type; D004095:Dihydropyridines; D017311:Amlodipine; C065927:cilnidipine