PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “PITUITARY HORMONES, POSTERIOR”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 127 records · Page 7Linked to original sources

[Experience with the use of posterior pituitary hormones in memory disorders of different etiology].

Results of using vasopressin and pituitrin in 20 patients with memory disturbances of various genesis (due to circulatory disturbances in the vertebrobasilar system, cerebral atherosclerosis, neurasthenia, brain concussion, epilepsy) are reviewed. The therapeutic efficacy of the hormones was evaluated with the use of a complex of psychophysiological methods. Objective changes in the patients' neurological status and subjective state were taken into account. A high therapeutic efficacy of the hormones in the treatment of amnestic syndromes is demonstrated.

Adult↗

Stimulus-induced depletion of pro-enkephalins, oxytocin and vasopressin and pro-enkephalin interaction with posterior pituitary hormone release in vitro.

The secretion of oxytocin (OXT) from the neurohypophysis is modulated by the actions of opioids acting via kappa-receptors. The vasopressin (AVP)-containing nerve terminals in the neurohypophysis contain the kappa-opioid agonist dynorphin, but endogenous opioid restraint of OXT secretion is observed even when AVP release is not activated, suggesting that another source of opioids is responsible for modulating OXT secretion. We now report that acute stimulation of the rat neural lobe in vivo results in depletion of the neural lobe content of OXT, AVP, dynorphin A1-17, dynorphin A1-8 and metenkephalin (Met-Enk). The dynorphin content is depleted to a similar extent as that of OXT and AVP; a correlation analysis suggests that while most dynorphin is co-secreted with AVP, a significant portion is co-secreted with OXT, consistent with a co-localisation of dynorphin with OXT. Met-Enk was depleted to a lesser extent than either hormone, consistent with a partial localisation in non-releasable pools. However, depletion of Met-Enk was also observed following naloxone-precipitated opioid withdrawal accompanying selective hypersecretion of OXT, suggesting co-secretion of OXT and Met-Enk. Met-Enk is a mu-opioid receptor agonist, but extended forms of Met-Enk, as we now report, are active at neurohypophysial kappa-receptors.

Animals↗