Influence of omega-Conotoxin GVIA, Nifedipine and Cilnidipine on Catecholamine Release in the Rat Adrenal Medulla.
- Author:
Byung Sik YU
1
;
Byeong Cheol KIM
;
Dong Yoon LIM
Author Information
1. Department of Anesthesiology, College of Medicine, Chosun University, Gwangju 501-759, Korea.
- Publication Type:Original Article
- Keywords:
Cilnidipine;
Nifedipine;
omega-conotoxin GVIA;
Catecholamine release;
Adrenal medulla;
Voltage-dependent Ca2+ channels
- MeSH:
(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethylammonium Chloride;
3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester;
Adrenal Glands;
Adrenal Medulla*;
Animals;
Calcium Channels;
Calcium Channels, L-Type;
Calcium Channels, N-Type;
Chromaffin Cells;
Dimethylphenylpiperazinium Iodide;
Membranes;
Nifedipine*;
omega-Conotoxin GVIA*;
omega-Conotoxins*;
Rats*;
Veins
- From:The Korean Journal of Physiology and Pharmacology
2007;11(1):21-30
- CountryRepublic of Korea
- Language:English
-
Abstract:
The present study was designed to establish comparatively the inhibitory effects of cilnidipine (CNP), nifedipine (NIF), and omega-conotoxin GVIA (CTX) on the release of CA evoked by cholinergic stimulation and membrane depolarization from the isolated perfused model of the rat adrenal medulla. CNP (3 micrometer), NIF (3 micrometer), and CTX (3 micrometer) perfused into an adrenal vein for 60 min produced greatly inhibition in CA secretory responses evoked by ACh (5.32 x 10(-3) M), DMPP (10(-4) M for 2 min), McN-A-343 (10(-4) M for 2 min), high K+ (5.6 x 10(-2) M), Bay-K-8644 (10(-5) M), and cyclopiazonic acid (10(-5) M), respectively. For the CA release evoked by ACh and Bay-K-8644, the following rank order of potency was obtained: CNP > NIF > CTX. The rank order for the CA release evoked by McN-A-343 and cyclopiazonic acid was CNP > NIF > CTX. Also, the rank orders for high K+ and for DMPP were NIF > CTX > CNP and NIF > CNP > CTX, respectively. Taken together, these results demonstrate that all voltage-dependent Ca2+ channels (VDCCs) blockers of cilnidipine, nifedipine, and omega-conotoxin GVIA inhibit greatly the CA release evoked by stimulation of cholinergic (both nicotinic and muscarinic) receptors and the membrane depolarization without affecting the basal release from the isolated perfused rat adrenal gland. It seems likely that the inhibitory effects of cilnidipine, nifedipine, and omega-conotoxin GVIA are mediated by the blockade of both L- and N-type, L-type only, and N-type only VDCCs located on the rat adrenomedullary chromaffin cells, respectively, which are relevant to Ca2+ mobilization. It is also suggested that N-type VDCCs play an important role in the rat adrenomedullary CA secretion, in addition to L-type VDCCs.
