Effects of and the Mechanism of Action of Calcium Antagonists and other Antianginal Agents

Author(s):  
A. Fleckenstein ◽  
G. Fleckenstein-Grün
2001 ◽  
Vol 82 (2) ◽  
pp. 132-133
Author(s):  
R. A. Giniatullin ◽  
R. R. Giniatullina ◽  
E. M. Sokolova ◽  
R. S. Garaev ◽  
A. O. Vizel

Intracellular ionized calcium ([Ca2 +] i) - ICIC - is a universal secondary messenger. The physiological signal leading to an increase in its level may be the action of hormones, mediators, trophic agents and other factors. A change in its level may underlie the mechanism of action of a number of drugs. However, until now, only calcium antagonists have become known, which inhibit the entry into the cell of extracellular FCCI. At the end of the 80s, modern methods for registering VKIK were proposed using highly sensitive non-toxic intracellular dyes that change the fluorescent signal with an increase in the concentration of ionized calcium in the cell. This opened up new opportunities for in-depth study of the mechanism of the effect of drugs on the dynamics of intracellular calcium.


1979 ◽  
Vol 57 (4) ◽  
pp. 348-358 ◽  
Author(s):  
Lois B. Rosenberger ◽  
D. J. Triggle

The cation ionophore A 23187 behaves similarly to the potent muscarinic agonist, cis-2-methyl-4-dimethylaminomethyl-1,3-dioxolane methiodide (CD) in guinea pig ileal longitudinal smooth muscle generating contractile responses that are gradedly sensitive to the concentrations of Ca2+ext and Na+ext. A 23187 and CD responses are insensitive to tetrodotoxin and A 23187 responses are insensitive to atropine. The responses to CD, A 23187, and veratridine are all similarly sensitive to the calcium antagonists D 600 and BAY-1040. D 600 failed to antagonize the ability of A 23187 to transport Ca2+ in a toluene-butanol: water two-phase system. It is suggested that in guinea pig ileal smooth muscle A 23187 does not translocate Ca2+ext exclusively but serves also to activate Ca2+ channels perhaps by an initial depolarizing Na+ entry.


2009 ◽  
Vol 215 (S681) ◽  
pp. 11-24 ◽  
Author(s):  
K.-E. Andersson ◽  
E.D. Högestätt

1977 ◽  
Author(s):  
J. Hladovec

On the basis of a new test for counting circulating endothelial cells in blood, a group of drugs was redefined which prevent endothelial desquamation after a standard intravenous injection of citrate into rats. The group comprised practically all drugs designated as venotonics or vitamin P-active agents, including some haemostatics, analgesic-antipyretics (acetylsalicylic acid) and some antiatherosclerotics (pyridinolcarbamate, Clofibrate). A marked activity was observed also with several calcium-antagonists (nifedipine, prenylamine, chromonar, dipyridamole and verapamil). Many endothelotropic drugs are simultaneously effective in blocking platelet functions. The suggested common mechanism of action is the influence on the consistency of the cellular surface coat (endothelia cement).


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