Studies on the calcium antagonistic action of tetrandrine: IX. Effects of tetrandrine on contractility of isolated swine coronary artery strips

Jia Ju-fang , Gao Nan-nan , Xia Guc-jin , Luo Qi-fa , Fang Da-chao , Jiang Ming-xing

Current Medical Science ›› 1985, Vol. 5 ›› Issue (4) : 15 -19.

PDF
Current Medical Science ›› 1985, Vol. 5 ›› Issue (4) : 15 -19. DOI: 10.1007/BF02856904
Article

Studies on the calcium antagonistic action of tetrandrine: IX. Effects of tetrandrine on contractility of isolated swine coronary artery strips

Author information +
History +
PDF

Abstract

Tetrandrine (Tet) 64 μM and verapamil (Ver) 8.4 μM relaxed the contraction of coronary artery strips. It is reversed by raising the extracellular Ca++ from 2.7 to 14.4 mM. Within a certain range (Tet 0. 1 μM 0.1 mM, Ver 1 nM 1 μM) the percentage of relaxation was in proportion to the dose. However, Tet and Ver exert no significant inhibition on the extracellular Ca++-dependent contraction induced by norepinephrine (NE). Probably Tet and Ver primarily inhibited the potential-dependent channel (PDC) and prevented the influx of Ca++ through PDC.

Tet 10 μM and Ver 0.1 μM also inhibited the release of intracellular Ca++ by NE. This shows that Tet and Ver might affect the transport of the intracellular Ca++. The relaxant effect of isoproterenol on the coronary strips was not blocked by Tet and Ver. Tet is therefore considered to be different from the β-blocker propranolol but similar to the calcium antagonist Ver.

Keywords

tetrandrine / iproveratril / Ca++ channel blockers / high K+ / norepinephrine / isoproterenol / swine coronary artery strip

Cite this article

Download citation ▾
Jia Ju-fang, Gao Nan-nan, Xia Guc-jin, Luo Qi-fa, Fang Da-chao, Jiang Ming-xing. Studies on the calcium antagonistic action of tetrandrine: IX. Effects of tetrandrine on contractility of isolated swine coronary artery strips. Current Medical Science, 1985, 5(4): 15-19 DOI:10.1007/BF02856904

登录浏览全文

4963

注册一个新账户 忘记密码

References

[1]

1981; 2(3): 163–6.

[2]

1982; (3)4: 233–6.

[3]

1982; 3(1): 97–101.

[4]

1958; 6(3): 147–53.

[5]

1983; 4(2): 130–3.

[6]

1983; 12(4): 373–5.

[7]

1983; 4(3): 230–9.

[8]

Fleckenstein A. On the Basic Pharmacological Mechanism of the Nifedipine and its Relation to Therapeutic Efficacy. Ins Jatene AD, Lichtlen PR, eds. 3rd International Adalat Symposium. Excerpta Medica 1976; 1–13.

[9]

BayerBL, et al. . Characterization of the adrenoceptors in coronary arteries of pigs. Eur J Pharmacol, 1974, 29(1): 58-65

[10]

Fleckenstein G, Fleckenstein A. Calciumantagonismus. In: Fleckenstein A, Roskamm H, eds. Berlin; 1980: 191–220.

[11]

GrünG, FleckensteinA. Die elektromechanische Entkoppelung der glatten Gefäßmuskulatur als Grundprinzip der Coronardilatation durch 4-(2′-Nitrophenyl)-2,6-dimethyl-1,4-dihydropyridin-3,5-dicarbonsäure-dimethylester (Bay a 1040, Nifedipine). Arzneimittelforsch, 1972, 22(2): 334-44

[12]

MeisheriKD, et al. . Evidence for two separated Ca++ pathways in smooth muscle plasmalemma. J Membr Biol, 1981, 59(1): 19-25

[13]

Van BreemenC, et al. . Ca++ movements in smooth muscle. Chest, 1980, 78(Suppl 1): 157-65

[14]

BroekaertA, GodfraindT. A comparison of the inhibitory effect of cinnarizine and papaverine on the noradrenaline and calcium-evoked contraction of isolated rabbit aorta and mesenteric arteries. Eur J Pharmacol, 1979, 53(3): 281-8

[15]

HaeuslerG. Differential effect of verapamil on excitation-contraction coupling in smooth muscle and on excitation-secretion coupling adrenergic nerve terminals. J Pharmacol Exp Ther, 1972, 180673-82

AI Summary AI Mindmap
PDF

88

Accesses

0

Citation

Detail

Sections
Recommended

AI思维导图

/