[Effect of neurotoxins on the electrical activity and contraction of the heart muscle]

Abstract

The goal of the present review is to report the effect of the main neurotoxins known on the electrical and mechanical activity of heart muscle. Toxins which block the sodium channel (tetrodotoxin, saxitoxin) shorten the action potential (AP) duration and decrease the initial depolarizing phase of the AP. Toxins which occupy different sites in the channel and alter the gating mechanisms of the Na channel (aconitine, batrachotoxin, veratridine, sea anemone and scorpion toxins, brevetoxin and ciguatoxin) depolarize, lengthen the AP duration, increase the contraction and cause arrhythmias. Ca channel agonists (atrotoxin, maitotoxin) increase the amplitude of the cardiac plateau. Ca channel antagonists (TCX, omega-conotoxin) decrease the magnitude of the plateau and exert a negative inotropic effect. Okadaic acid increases the Ca current leading to an increase in the plateau amplitude and a lengthening in the AP duration and the development of a positive inotropic effect on the contraction. Toxin affecting voltage-dependent K channels on heart muscle and the actual knowledge concerning the effect and the mode of action of palytoxin have also been reviewed. It is concluded that toxins, used as tools to analyze and characterize the structure and the function of ionic channels involved in the development of the electrical activity of excitable cells exhibit numerous effects on cardiac muscle. Some of these effects might not only be due to a direct action of these substances on membrane channels but they might also be the result of the release of neuromediators from nervous endings surrounding cardiac cells.