モリモト　サトシ   Morimoto Satoshi   森本　聡    所属   医学部 医学科（東京女子医科大学病院）    職種   准教授
論文種別	原著
言語種別	英語
査読の有無	査読あり
表題	Effects of efonidipine hydrochloride on heart rate and circulatory changes due to stress.
掲載誌名	正式名：Clinical and experimental hypertension (New York, N.Y. : 1993) 略　 称：Clin Exp Hypertens ISSNコード：15256006/10641963
掲載区分	国外
巻・号・頁	31(1),pp.83-91
著者・共著者	Morimoto Satoshi†*, Jo Fusakazu, Maki Kei, Iwasaka Toshiji
担当区分	筆頭著者,責任著者
発行年月	2009/02
概要	Efonidipine hydrochloride is a dual Ca channel blocker that inhibits T-type Ca channels, which are localized in the sinoatrial node and are involved in the pacemaker mechanism of the heart, as well as L-type Ca channels. In the present study, the effect of efonidipine hydrochloride in inhibiting an increase in heart rate along with changes in circulation during mental and physical stress was examined using normotensive volunteers. A mental arithmetic test caused significant increases in heart rate and blood pressure, which were significantly inhibited 3 hours after oral administration of 40 mg of efonidipine hydrochloride but not at 1 week after cessation of administration. In contrast, the plasma norepinephrine, epinephrine, renin activity, and aldosterone levels following the test were unchanged at both 3 hours and 1 week after administration of efonidipine hydrochloride. Physical stress in the form of cold by immersing one hand in ice water for 2 minutes induced similar increases in the heart rate and blood pressure, which were significantly reduced at 3 hours but not at 1 week after administration of efonidipine hydrochloride. The plasma levels of the humoral factors previously described following the physical stress were unchanged at either 3 hours or 1 week after administration of efonidipine hydrochloride. These results suggest that efonidipine hydrochloride inhibits increases in heart rate and blood pressure due to stress, presumably by blocking T-type Ca channels rather than by inhibiting the sympathetic nervous system. Therefore, efonidipine hydrochloride is expected to be a Ca antagonist that exhibits a strong cardioprotective effect.
DOI	10.1080/10641960802627363
PMID	19172462