Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P01178 (oxytocin)
 15,767 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A solution hybridization/RNase protection assay for the molar quantitation of vasopressin and oxytocin mRNAs, using synthetic complementary RNA probes, is described. This assay was optimized to permit the identification of vasopressin (AVP) mRNAs containing the frame-shift point deletion causing inheritable diabetes insipidus in the Brattleboro strain of rat. Examination of RNA from hypothalamic magnocellular tissue punches found that of the 86.1 x 10(-18) mol [86.1 attomoles (amol)] of AVP mRNA detected in the Brattleboro heterozygote paraventricular (PVN) nucleus, 5.2% could be shown to be mutant AVP mRNA (AVPd RNA). The percentage of AVPd RNA increased dramatically to 18.1% after 6 d of chronic intermittent salt-loading. Similar percentages and percentage increases of AVPd RNA were detected in the heterozygote supraoptic nucleus (SON). These values were contrasted with those found in parallel studies in both Long Evans and Brattleboro homozygotes, and compared with values for oxytocin (OT) mRNA in all 3 AVP rat genotypes. The results of continued osmotic regulation of the mutant AVP gene, the low native levels of AVPd RNA found in both the Brattleboro heterozygote and homozygote, and the magnitudes of AVPd expression change with chronic osmotic challenge were interpreted as indicating that (1) in the diploid rat genome, both AVP alleles are transcribed, (2) the osmotic regulation of the mutant AVP gene is normal, and (3) the low levels of AVPd mRNA are consistent with a shorter-than-control effective mRNA half-life.
 ...
PMID:Differential expression of vasopressin alleles in the Brattleboro heterozygote. 319 79

Regeneration and functional recovery of the hypothalamoneurohypophysial system (HNS) in neurohypophysectomized rats treated with either saline or vasopressin (VP) were analyzed utilizing specific immunohistochemical and physiological measures. Neural lobe ablation combined with VP administration precipitated a profound diabetes insipidus (following cessation of VP delivery) that persisted for the duration of the experiment. Diabetes insipidus was correlated with a drastic reduction in the number of VP-positive neurons in magnocellular hypothalamic nuclei. In contrast, large numbers of oxytocin (OT)-positive neurons survived neurohypophysectomy in VP-treated neurohypophysectomized rats; OT neurons accounted for the vast majority of magnocellular profiles observed in Nissl-counterstained sections. VP-immunoreactive fibers could be observed in limited quantities in the external lamina of the median eminence of VP-treated neurohypophysectomized rats, with little staining evident in the internal lamina. Saline-treated neurohypophysectomized rats exhibited the recovery of antidiuretic function characteristically seen following this lesion, with evidence of survival of considerable numbers of VP and OT neurons and median eminence hypertrophy. Both the internal and external laminae of the median eminence were densely innervated by large-caliber VP and OT fibers. Sham-operated animals receiving VP treatment did not show any long-term deficit in water metabolism, changes in the complement of VP or OT perikarya in hypothalamus, or changes in the innervation of the median eminence. Results indicate that VP treatment following neurohypophysectomy results in extensive retrograde degeneration of magnocellular VP neurons without affecting the survival of OT cells.
 ...
PMID:Selective cell death of magnocellular vasopressin neurons in neurohypophysectomized rats following chronic administration of vasopressin. 330 29

Previous studies have shown a disappearance of interstitial cells from the renal medulla of rats with hereditary diabetes insipidus (Brattleboro) when the animals were treated with vasopressin in high doses. The present study was undertaken to elucidate the mechanisms behind this cell loss. The disappearance of interstitial cells from the renal medulla of Brattleboro rats was quantitatively determined by electron microscopic stereology after various types of treatment. A considerable decrease in the volume density of interstitial cells was induced by the administration of either 8-arginine vasopressin or 1-desamino-8-D-arginine vasopressin. This lesion of the interstitial cells was not prevented by the simultaneous administration of oxytocin. Even a 48-hour period of water deprivation also resulted in a slight decrease in the volume density of interstitial cells. The results indicate that the observed loss of renal medullary interstitial cells is not a direct effect of the hormone on the cells but probably secondary to the marked increase in the renal medullary solute (urea) concentration. The fact that animals with hardly any renomedullary interstitial cells concentrated their urine to a virtually normal level shows that these cells cannot play an important role in the concentrating mechanism. The interstitial cells recovered rapidly when the vasopressin treatment was discontinued, but it could not be determined whether this was due to local proliferation or to the immigration of cells from extrarenal tissue.
 ...
PMID:Loss of renomedullary interstitial cells in Brattleboro rats after vasopressin treatment. 335 33

Cysteamine (beta-mercaptoethylamine, CSH) has been reported to have various effects on the neuroendocrine system. Reports indicate CSH decreases pituitary oxytocin (OT) without affecting pituitary vasopressin (VP). However, preliminary studies from our laboratory strongly indicate that CSH has an effect on VP release. Experiments were conducted with dibenzyline-treated, urethane-anesthetized, male Sprague-Dawley (SD) rats. Rats were injected with 4 mU of standard VP and 4 mg/100 g of CSH. Administration of VP resulted in an increase in mean arterial pressure (MAP) of 23.5 +/- 3.2 mm Hg. Administration of CSH resulted in a consistent, immediate decrease in MAP of 13.0 +/- 2.0 mm Hg prior to an increase of 21.0 +/- 2.6 mm Hg. The effects due to VP and CSH were strikingly different; the CSH-induced MAP rise took longer to peak and to return to baseline. Both the VP- and CSH-induced MAP rise were markedly inhibited by a prior administration of a specific VP antagonist d(CH2)5[Tyr(Me)]AVP. In addition, the typical increase in MAP observed in SD rats following CSH administration was substantially reduced when the same dose was administered in homozygous diabetes insipidus (HODI) rats. The data presented here strongly suggest that CSH-induced MAP elevation is due to the release of VP from the pituitary gland.
 ...
PMID:Effects of cysteamine on blood pressure: possible mediation through vasopressin release. 342 Jan 12

A case of a pregnant woman with diabetes insipidus is reported. The course of the pregnancy was uneventful except for a slightly increased need for vasopressin during the last trimester. Neurophysin levels increased at a rate similar to that seen in the normal pregnant state. The combination of normal neurophysin physiology and undisturbed spontaneous labor demonstrating normal oxytocin secretion suggests that there is a singular deficiency of antidiuretic hormone in essential diabetes insipidus.
 ...
PMID:Diabetes insipidus and pregnancy. 342 73

In order to study putative hypothalamic mechanisms of sleep waking cycle regulation we destroyed, by electrolytic coagulation, a large part of the medial hypothalamus overlapping the paraventricular nucleus in 6 adult cats. We never observed any modification of light slow wave sleep. Three of the six cats presented no paradoxical sleep (PS) impairment, despite an almost total destruction of neurophysin-immunoreactive cells of PVN in two cats and marked signs of diabetes insipidus in the third. Further, in the other three animals a statistically significant decrease of daily quantities of PS and deep slow wave sleep (SWS2) were related to an extensive destruction of the anterior hypothalamic area. These results suggest lack of influence of the PVN in sleep regulation and an involvement of the anterior hypothalamus in the onset of SWS2 and PS.
 ...
PMID:Effects of electrolytic lesion of hypothalamic paraventricular nucleus and its related areas on the sleep waking cycle in the cat. 343 26

Vasopressin and oxytocin exert pronounced effects on behaviour by a direct action on the brain. A single injection of vasopressin results in a long-term inhibition of extinction of a conditioned avoidance response suggesting that vasopressin triggers a long-term effect on the maintenance of a learned response, probably by facilitation of memory processes. In addition vasopressin improves passive avoidance behaviour, delays extinction of appetitive discrimination tasks, affects approach behaviour to an imprinting stimulus in ducklings, improves copulation rewarded behaviour of male rats in a T-maze, prevents or reverses amnesia induced by electroconvulsive shock, CO2 inhalation, pentylenetetrazol or puromycin. The majority of these effects of vasopressin in the various and sometimes relatively complex tasks may be explained by stimulatory influences of this neuropeptide on memory processes. Generally oxytocin exerts effects which are opposite to those of vasopressin and it has been suggested that oxytocin may be an amnesic neuropeptide. Various limbic system structures seem to act as the anatomical substrate for the behavioural effects of vasopressin. In particular the amygdala, the dentate gyrus of the hippocampal complex, the ventral hippocampus and the dorsal septum seem to be involved. Evidence has been obtained from experiments with homozygous diabetes insipidus rats and from experiments in which antisera were applied that endogenous vasopressin and oxytocin play a physiological role in brain processes related to memory. It appears that highly active fragments can be generated from vasopressin and experiments in which a fragment of vasopressin ([pGlu4, Cyt6]AVP-(4-8)) as well as an AVP-antagonist were used, reveal that the vasopressin receptors mediating the behavioural effects are situated in the brain and differ in specificity from the peripheral (blood pressure) vasopressin receptors. Generally the clinical data obtained so far with vasopressin treatment are in agreement with the results from animal experiments and they support the notion on the involvement of vasopressin in memory function. The sometimes reported conflicting results on vasopressin effects in certain patients (Korsakoff or Alzheimer) may have to do with the wide-spread pathology in these diseases.
 ...
PMID:Vasopressin and oxytocin. Their presence in the central nervous system and their functional significance in brain processes related to behaviour and memory. 346 10

In order to investigate the possible role of oxytocin in osmoregulation and its response to stress, plasma immunoreactive oxytocin was measured during hypertonic saline infusion and insulin-induced hypoglycaemia in a group of normal subjects, four patients with idiopathic diabetes insipidus and one patient with DIDMOAD syndrome (the syndrome of diabetes insipidus, diabetes mellitus, optic atrophy and deafness). The results were compared with those of plasma immunoreactive vasopressin to the same stimuli. As expected, there was a rise in plasma vasopressin in the normal subjects to both tests: this was absent in the patients with diabetes insipidus. Plasma oxytocin did not rise during hypertonic saline infusion in either group of subjects. The response of oxytocin to insulin-induced hypoglycaemia (0.15 U/kg soluble insulin) in normal subjects was much more variable. One highly symptomatic volunteer showed a marked rise in oxytocin. Two subjects also showed a rise when retested with 0.19 U/kg soluble insulin. There was no response of oxytocin to a standard-dose insulin test in the patients with diabetes insipidus. The data suggest that, in man, oxytocin is not involved in osmoregulation but that it may be secreted in response to marked hypoglycaemia.
 ...
PMID:Responses of neurohypophysial peptides to hypertonic saline and insulin-induced hypoglycaemia in man. 351 6

Neurohypophyseal function has been investigated in 11 children undergoing pituitary or suprasellar surgery. All had corticosteroid and thyroxine replacement; 9 developed diabetes insipidus (DI) within 1-12 h of operation. At the onset of DI, the plasma vasopressin (AVP) concentration was 3.9 +/- 1.2 pmol/l, considerably higher values usually associated with cranial DI (less than 0.9 pmol/l). AVP fell significantly to 1.1 +/- 0.2 pmol/l by the second day of DI. There was a similar change of levels of the AVP prohormone/carrier peptide, neurophysin I, but plasma oxytocin did not change significantly. High performance liquid chromatography of plasma at the onset of DI revealed a major peak that coeluted with synthetic AVP and two smaller peaks of AVP immunoreactivity. Seven patients required very large doses of desamino-8-D-arginine vasopressin (DDAVP) during the first day; 4 needed smaller doses on day 2. Water deprivation tests were performed on days 6 and 14 after operation in 5 patients with prolonged DI (2 with a triple response). There were no differences in plasma AVP on the two occasions but urinary AVP excretion rate was significantly higher on day 6 (2.4 +/- 0.8 pmol/h) than day 14 (0.7 +/- 0.3 pmol/h). It is concluded that early postoperative DI is not due to decreased levels of circulating AVP but may be related to the release of biologically inactive precursors from the damaged neurohypophysis. These may lead to renal refractoriness to AVP. There is a higher urinary AVP excretion rate on day 6 than day 14 after operation in both patients with a triple response and those with uninterrupted DI. Other factors may determine whether or not a transient resolution phase of DI occurs.
 ...
PMID:Neurohypophyseal peptide function during early postoperative diabetes insipidus. 358 Aug 32

The de Morsier syndrome, or septo-optic dysplasia, is a developmental anomaly characterized by involvement of the optic system, hypothalamic-pituitary axis and septum pellucidum. Only a few anatomical observations are recorded. We report three new cases and review the pertinent literature. The neuropathological lesions varied as did the clinical features. The hypothalamic nuclei were most commonly involved, followed by the optic system and the septum pellucidum. Other lesions were found in the cerebral cortex, corpus callosum, olfactory system and cerebellum. The hypopituitarism appeared to have been secondary to hypothalamic damage rather than to intrinsic pituitary defect. A virtually normal histology and the usual endocrine cell populations were demonstrated by immunocytochemistry in the adenohypophysis. Damage to the neurophysin-containing cells of the hypothalamus explains the various degrees of clinically observed diabetes insipidus.
 ...
PMID:Neuropathology of "septo-optic dysplasia" (de Morsier syndrome) with immunohistochemical studies of the hypothalamus and pituitary gland. 362 36


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>