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

It is one of the most important achievements in modern basic cardiology that many substances with a positive or negative inotropic effect on heart muscle act as promoters or inhibitors of the mediator function of Ca2+-ions in excitation—contraction coupling. For instance, s-adrenergic stimulation with adrenaline, nor-adrenaline, or isoproterenol facilitates the transmembrane Ca2+ influx during excitation. Splitting of ATP by the Ca2+-activated myofibrillar ATPase, and contractile tension development, are thereby augmented. Similarly, under the influence of cardiac glycosides, more Ca2+ is made available to the contractile myofibrils. Conversely, a number of negative isotropic substances can inhibit excitation—contraction coupling of heart muscle by a Ca2+- antagonistic effect.