Comparison of Inhibitory Effects between Enalapril and Losartan on Adrenal Catecholamine Secretion.
10.5646/jksh.2014.20.2.51
- Author:
Hyo Jeong LIM
1
;
Young Youp KOH
;
Dong Yoon LIM
Author Information
1. Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Veterans Health Service Medical Center, Seoul, Korea.
- Publication Type:Original Article
- Keywords:
Enalapril;
Losartan;
Catecholamine secretion;
Adrenal medulla;
angiotensin II type-1 receptor blocker;
Angiotensin-converting enzyme inhibitor
- 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;
Acetylcholine;
Adrenal Glands;
Adrenal Medulla;
Ammonium Compounds;
Angiotensin II;
Animals;
Catecholamines;
Cytoplasm;
Dimethylphenylpiperazinium Iodide;
Enalapril*;
Losartan*;
Perfusion;
Rats;
Veins;
Veratridine
- From:Journal of the Korean Society of Hypertension
2014;20(2):51-67
- CountryRepublic of Korea
- Language:English
-
Abstract:
BACKGROUND: The present study was attempted to compare enalapril, an angiotensin-converting enzyme inhibitor with losartan an angiotensin II (Ang II) receptor blocker in the inhibitory effects on the secretion of catecholamines (CA) from the perfused model of the rat adrenal gland. METHODS: The adrenal gland was isolated and perfused with Krebs-bicarbonate. CA was measured directly by using the fluorospectrophotometer. RESULTS: Both enalapril and losartan during perfusion into an adrenal vein for 90 minutes inhibited the CA release evoked by acetylcholine (ACh), 1.1-dimethyl-4-phenyl piperazinium (DMPP, a selective Nn agonist), high K+ (a direct membrane-depolarizer), 3-(m-chloro-phenyl-carbamoyl-oxy-2-butynyl-trimethyl ammonium (McN-A-343, a selective M1 agonist), and Ang II in a time-dependent manner. Also, in the presence of enalapril or losartan, the CA release evoked by veratridine (an activator of voltage-dependent Na+ channels), 6-dimethyl-3-nitro-4-(2-trifluoromethyl-phenyl)-pyridine-5-carboxylate (BAY-K-8644, an L-type Ca2+ channel activator), and cyclopiazonic acid (a cytoplasmic Ca2+-ATPase inhibitor) were significantly reduced. Based on the same concentration of enalapril and losartan, for the CA release evoked by ACh, high K+, DMPP, McN-A-343, Ang II, veratridine, BAY-K-8644, and cyclopiazonic acid, the following rank order of inhibitory potency was obtained: losartan > enalapril. In the simultaneous presence of enalapril and losartan, ACh-evoked CA secretion was more strongly inhibited compared with that of enalapril- or losartan-treated alone. CONCLUSIONS: Collectively, these results demonstrate that both enalapril and losartan inhibit the CA secretion evoked by activation of both cholinergic and Ang II type-1 receptors stimulation in the perfused rat adrenal medulla. When these two drugs were used in combination, their effects were enhanced, which may also be of clinical benefit. Based on concentration used in this study, the inhibitory effect of losartan on the CA secretion seems to be more potent than that of enalapril.
