By Lionel H. Opie MD, PhD, FRCP, William A. Coetzee DSc (auth.)
Calcium antagonists at the moment are considered as crucial increase in cardiac drug treatment because the creation of beta-adrenergic blockading brokers. appearing ba sically as vasodilators-though with many different com plex mechanisms specifically when it comes to the anti arrhythmic calcium antagonists, those brokers have grown in value to turn into one of the healing brokers of first selection for angina pectoris and hyper stress. the main objective of the current publication is to give the clinician with the data wanted for the sensible use of calcium antagonists. What do the entire a number of and infrequently conflicting trials say? Do those brokers particularly paintings? if that is so, which agent and in what dose? How do the 3 entrance runners, verapamil, nifedipine and diltia zem evaluate within the efficacy and side-effects with one another? How do the hot moment new release brokers, now getting into the North American marketplace, fit in and com pare with the 3 first-liners? while the gloss is taken clear of the ads, what's rather left? The powerful medical bias of the current booklet could be complimented by means of additional analyzing of books slanted in the direction of basics. probably the most vital and up to date of those is that by means of Dr Winifred Nayler (Calcium Antagonists, educational Press, 1988). That booklet could be simple for crucial history wisdom within the zone of calcium antagonists. the real uncomplicated contribu tions of Fleckenstein deserve emphasis.
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Extra info for Clinical Use of Calcium Channel Antagonist Drugs
Am J PhysioI1981;24:H187H193. Vassort G, Rougier 0, Garnier D, et al. Effects of adrenaline on membrane inward currents during the cardiac action potential. Pflugers Arch 1969;309:70-81. Reuter H. Localization of beta adrenergic receptors, and effects of noradrenaline and cyclic nucleotides on action potentials, ionic currents and tension in mammalian cardiac muscle. J PhysioI1974;242:429-451. Reuter H, Scholtz H. The regulation of the calcium conductance of cardiac muscle by adrenaline. J Physiol1977; 264:49-62.
For site of action of calcium antagonists, see Figure 1-5. According to these concepts, calcium antagonists should relieve coronary artery spasm and ~-adrenergic blockers exaggerate the phenomenon. From Opie and Maseri (131]. (Figure copyright: LH Opie). to calcium antagonism , at least not in the aorta. Such internal calcium release system is theoretically unlikely to respond to calcium antagonism, as also supported by some (but not all) experimental evidence  . On the other hand, alpha-2-stimulation may evoke Ca 2+ influx which may be inhibited by calcium antagonists (Figure 1-5), depending on the type and site of blood vessel .
20 Coetzee dividual calcium channel can now be measured. There exist two types of calcium channels, a T-type (fast) which plays a role in pacemaker activity and the initiation of the action potential in nodal tissue, and a Ltype (slow) which is probably responsible for calcium entry during the plateau of the action potential. The calcium current is also modulated by neurotransmitters in normal physiologic conditions. Adrenaline, for example, increases the calcium current by increasing the probability of the calcium channel to be in the open state, while acetylcholine decreases the calcium current.