The effect of delta-sleep-inducing peptide on the Ca-transporting system of the sarcoplasmic reticulum and activity of the myocardial antioxidant enzymes

Abstract

It is demonstrated that immobilization stress against the background of lowered catalase activity impairs the function of the sarcoplasmic reticulum Ca pump, particularly at high Ca 2+ levels. The membranes of intraceltular Ca 2+ depots are destroyed much more rapidly than in the control, which results in Ca 2 § release. Administration of delta sleep-inducing peptide to control animals results in a 30% increase in catalase activity for an unchanged level of superoxide dismutase and markedly improves the function of the Ca-transporting system at elevated levels of free Ca 2 § A long-term stress after administration of the peptide not only causes no damage to the Ca-transporting system but actually increases its efficiency (compared with the control) at a high catalase level.Key Words: delta sleep-inducing peptide; Ca pump; sarcoplasmic reticulum; superoxide dismutase; myocardium Stress-induced damage to myocardial ion-transporting systems: sarcolemmal Na,K-ATPase [6] and sarcoplasmic reticulum Ca-ATPase [13] resulting from the activation of lipid peroxidation (LPO) can be prevented by central and peripheral stress-limiting systems of the organism [5]. Adaptation to a short-term stress, which can prevent disturbances of the electrical stability of the heart and arrhythmias in stress, ischemia, reperfusion, myocardial infarction, and postinfarction cardiosclerosis [14], is an example of combined activation of the central and peripheral stresslimiting systems of the organism. Adaptation to stress also prevents stress-induced damage to the Na,K pump [6] and optimizes the function of the Ca pump [13], i.e., it triggers a mechanism that operates at the level of the heart, limits arrhythmias, and protects against alterations in Ca homeostasis.An important role of delta sleep-inducing peptide (DSIP) in adaptation has recently been recognized. It has been shown that, in addition to normalizing sleep, this peptide activates the monoaminergic transmitter and serotoninergic systems and, being an opiate receptor agonist, displays antidepressant and analgetic activities [3,11]. DSIP raises the resistance of animals to emotional stress [7], prevents their death from cardiovascular disorders [4], and elicits an antiarrhythmic effect in emotional stress [8]. Moreover, it prevents stress-induced sleep disorders in rabbits [15]. Administration of DSIP and its analogs forestalls activation of LPO in acute pancreatitis and cold stress and stabilizes tysosomal membranes [10]. Thus, DSIP elicits both central and peripheral effects, regardless of the route of administration. However, its effect on the electrical stability of the heart devel-