Function of the hypothalamo-neurohypophysial system in rats with myocardial infarction is modified by melatonin.

BACKGROUND Pineal and melatonin interactions with the hypothalamo-neurohypophysial system are well documented. In addition, vasopressin and oxytocin secretion are known to be part of the neuroendocrine response to chronic heart failure evoked by myocardial infarction. The present study was undertaken to evaluate the possible regulatory role of melatonin in the vasopressin and oxytocin release in rats with myocardial infarction. METHODS The vasopressin and oxytocin content of the hypothalamus and neurohypophysis, as well as their plasma levels, were radioimmunoassayed in sham-operated or pinealectomized rats with left coronary artery ligation (CAL)-evoked myocardial infarction as well as under melatonin treatment. RESULTS Infarcted rats demonstrated increased vasopressin and oxytocin plasma levels, but melatonin restricted the release of both neurohormones in these rats. Experimental myocardial infarction in pinealectomized rats caused a distinct inhibition of vasopressin release but intensified oxytocin secretion. In pinealectomized rats substituted with melatonin, pineal indole amine was seen to inhibit oxytocin release and stimulate vasopressin secretion. CONCLUSIONS (i) CAL-induced myocardial infarction is the reason for increased hypothalamo-neurohypophysial system activity in rats; melatonin plays the role of inhibitory neuromodulator of vasopressin and oxytocin release in this state. (ii) Myocardial infarction evoked in pinealectomized rats is characterized by the inversion of the neurohumoral response pattern in respect of inhibited vasopressin release. (iii) Melatonin stimulates vasopressin (but decreases oxytocin) release in pinealectomized rats with myocardial infarction.