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자료유형
학술대회자료
저자정보
Lim, Dong-Yoon (Department of Pharmacology, College of Medicine) Woo, Seong-Chang (Department of Pharmacology, College of Medicine) Ko, Suk-Tai (Pharmacy, Chosun University)
저널정보
한국응용약물학회 한국응용약물학회 추계학술발표논문집 한국응용약물학회 2001년도 추계학술대회 및 정기총회
발행연도
2001.1
수록면
95 - 95 (1page)

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Ciinidipine (FRC-8635) is a newly synthesized novel DHP type of organic Ca$\_$2+/channel blockers that have been developed so far in Japan (Yoshimoto et al., 1991 : Hosono et at., 1992). It also has a blocking action on L-type voltage-dependent Ca$\^$2+/channel (VDCCs) in the rabbit basilar artery (Oike et al., 1990) and a slow-onset and long-lasting hypotensive action in clinical and experimental studies (Ikeda et al., 1992 ; Tominaga et al., 1997). Recent electrophysiological data indicate that cilnidipine might be a dual-channel antagonist for peripheral neuronal N-type and vascular L-type Ca$\^$2+/channels (Oike et al., 1990 ; Fujii et al., 1997; Uneyama et at., 1997). However, little is known about the involvement of N-type VDCCs in contributing to the muscarinic receptor-mediated CA secretion. Therefore, the present study was attempted to investigate the effect of cilinidipine on secretion of catecholamines (CA) evoked by ACh, high K$\^$+/, DMPP and McN-A-343 from the isolated perfused rat adrenal gland. Cilnidipine (1-10 ${\mu}$M) perfused into an adrenal vein for 60 min produced dose- and time-dependent inhibition in CA secretory responses evoked by ACh (5.32${\times}$10$\^$-3/M), DMPP (10$\^$-4/ M for 2 min) and McN-A-343 (10$\^$-4/ M for 2 min). However, lower dose of lobeline did not affect CA secretion by high K$\^$+/(5.6${\times}$10$\^$-2/ M), higher dose of it reduced greatly CA secretion of high K$\^$+/. Cilnidipine itself did also fail to affect basal catecholamine output. Furthermore, in adrenal glands loaded with cilnidipine (10 ${\mu}$M), CA secretory response evoked by Bay-K-8644 (10 ${\mu}$M), an activator of L-type Ca$\^$2+/channels was markedly inhibited while CA secretion by cyclopiazonic acid (10 ${\mu}$M), an inhibitor of cytoplasmic Ca$\^$2+/-ATPase was no affected. Moreover, $\omega$-conotoxin GVIA (1 ${\mu}$M), given into the adrenal gland for 60 min, also inhibited time-dependently CA secretory responses evoked by ACh and high K$\^$+/.

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