The hypothalamic nonapeptide
vasopressin is a known player in the pathogenesis of chronic
heart failure. According to the large body of clinical evidence,
vasopressin has an impact on
salt and water imbalance,
hyponatremia, and subsequent
renal insufficiency - the most common and destructive co-morbidity of patients afflicted with chronic
heart failure. Despite the well-documented elevated levels of
vasopressin in the blood of such patients, its expression in the magnocellular hypothalamic nuclei and transport to the posterior pituitary has not yet been investigated. In addition, the literature almost lacks the information on the contribution of another member of nonapeptide family,
oxytocin, in the pathogenesis of this disease. Here we present a postmortem analysis of
vasopressin and
oxytocin-immunoreactive neurons and their terminals in the posterior pituitary of 8 male patients (53.8+/-9.3 years) who had died from CHF and 9 male controls (54.6+/-11.8 years). In line with previous clinical reports, our study on hypothalami of chronic
heart failure patients revealed a significant increase in the relative profile density (+29%) of
vasopressin-positive neurons in the hypothalamic supraoptic nucleus. Consistently we found a significant increase in the relative optic density of
vasopressin-immunoreactivity in the posterior pituitary (+33%) of these patients. In contrast, the similar analysis applied for
oxytocin neurons revealed no statistically significant differences to controls. In conclusion, our study provides the morphological evidence for activation of
vasopressin (but not
oxytocin) expression and
vasopressin transport to the posterior pituitary in patients with chronic
heart failure.