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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Physical injury of any sort--accidental injury, burns or elective surgery--provokes an immediate neuroendocrine response. Neural input arising from the cerebral cortex, damaged tissues and receptors detecting fluid loss leads to increased secretion of ACTH, growth hormone, prolactin and vasopressin from the pituitary, and to a general activation of the sympathetic nervous system, with rises in adrenaline and noradrenaline concentrations. Secondary changes include stimulation of cortisol and aldosterone and inhibition of insulin and somatomedin secretion. The glucagon concentration and plasma renin activity may also be increased, either immediately or after a delay. The duration of these responses generally depends upon the severity of the injury and differs considerably between hormones, for reasons that are not understood. The only endocrine changes consistently seen at later times after trauma are an increase in insulin secretion, which supersedes the initial suppression, and decreases in the concentrations of T3 and gonadal steroids. Some of the changes in steroid, thyroid and pancreatic hormones differ temporally or even qualitatively from those of their usual stimuli and are unexplained. The initial neuroendocrine response to injury can be construed as playing a defensive role, but the function of the later changes is not understood; it seems likely that they are adaptive in nature, but the scope for therapeutic intervention remains unclear.
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PMID:The neuroendocrinology of physical injury. 332 96

Basal plasma concentrations of growth hormone (GH) were monitored in both normal and estradiol-primed male rats by the collection of sequential blood samples from freely moving rats, via chronic intraatrial cannulae. Blood was sampled every 2 min for a period of 80 min and plasma GH levels determined by radioimmunoassay. The normal male rats displayed a pulsatile release of GH, while the estradiol-primed male rats exhibited a relatively steady level of plasma GH concentration. The rats exposed to high levels of estradiol (1.59 +/- 0.42 nmol/l plasma) also had a higher mean value of basal GH concentration. An injection of 100 micrograms/kg of bovine neurophysin II did not alter GH release in the normal male rats. However, it did significantly elevate GH levels in the estradiol-primed animals to a mean peak level approximately six times the mean basal level. The administration of 100 micrograms/kg of bovine neurophysin I to estradiol-primed male rats did not produce any change in plasma GH levels and thus eliminates the possibility of the nonspecific stimulation of neurophysin II on GH release.
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PMID:Bovine 'neurophysin II' stimulates growth hormone release in the estradiol-primed male rat. 334 67

The present study examines the effects of auditory stress on the plasma levels of pituitary hormones and cortisol. Each of twelve healthy male subjects participated in two experimental series; during one of them they were exposed to 85 dB(A) industrial noise from 9:00 to 21:00 h. Blood samples were taken by an indwelling venous catheter for 24 h at intervals of 20 min from 8:00 to 8:00 h. The plasma levels of ACTH, growth hormone, prolactin, oxytocin, vasopressin and cortisol were determined. In all subjects except one noise stress affected the profiles of the pituitary hormones but the responses were interindividually different. The oxytocin level was significantly elevated (p less than .01), ACTH also responded but less clearly, whereas the other hormones reacted only in individual cases. During the subsequent night sleep only PRL concentrations were elevated above the baseline plateau in several subjects. It was concluded that in humans the pituitary responses to noise stress are highly individual.
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PMID:Effects of daytime noise load on the sleep-wake cycle and endocrine patterns in man: II. 24 hours secretion of anterior and posterior pituitary hormones and of cortisol. 341 Jun 40

The effect of clonidine (4.5 micrograms kg-1) on haemodynamics and hormonal stress responses was evaluated in 21 female patients undergoing breast surgery. The standardized general anaesthesia included diazepam as premedicant, thiopentone, enflurane, N2O, fentanyl and vecuronium. Venous plasma concentrations of noradrenaline, adrenaline, growth hormone, vasopressin, and cortisol were assayed at various times before, during and after surgery. Clonidine attenuated the sympathoadrenal response; arterial blood pressure and heart rate increases in association with intubation were lower in clonidine-premedicated patients. Noradrenaline levels were lower throughout and 3 h after surgery in the clonidine group (P less than 0.05). Adrenaline levels were lower in this group 2 min after intubation (P less than 0.05). Growth hormone, vasopressin and cortisol plasma levels were increased at the end of and after surgery, with no differences between the groups. In spite of the effect on sympathoadrenal response, clonidine did not have any significant additive anxiolytic effect. Statistically significant differences were not found as to need for postoperative analgesics.
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PMID:Oral premedication with clonidine: effects on stress responses during general anaesthesia. 343 64

Since neuroimmunomodulation is brought about in part, at least, by secretion of pituitary hormones involved in stress and immune responses, we review briefly the hypothalamic control of the release of ACTH, growth hormone, and prolactin. The release of ACTH is controlled particularly by corticotropin-releasing factor (CRF), but vasopressin has intrinsic releasing activity and potentiates the action of CRF at both hypothalamic and pituitary levels. Oxytocin may even potentiate the action of CRF, but has little, if any, ACTH-releasing activity by itself. In addition, epinephrine may augment responses to the CRFs. In contrast, growth hormone is under dual control by growth-hormone-releasing factor (GRF) and somatostatin, and prolactin is under multifactorial control by a series of inhibitors and stimulators. Dopamine is accepted as a physiological prolactin-inhibiting factor (PIF), but probably GABA and possibly acetylcholine as well are PIFs. There is good evidence for a peptide PIF as well. There are a number of prolactin-releasing factors (PRFs) which include oxytocin, vasoactive intestinal polypeptide, PHI and TRH. Several other peptides can also release prolactin, including angiotensin II. In response to stress there is a complex interaction of peptides intrahypothalamically. CRF augments its own release by an ultra short-loop positive feedback, and there is negative ultra short-loop feedback of GRF and somatostatin. Vasopressin appears to augment CRF release as well as to act directly on the pituitary, and there are complex interactions of various peptides to influence prolactin and GH release.
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PMID:The role of brain peptides in neuroimmunomodulation. 347 67

Following intraventricular (i.v.t.) administration of increasing doses of neuropeptide Y (NPY; 7.5-750 pmol/rat) the catecholamine levels and turnover were quantitatively measured in discrete hypothalamic regions by means of histofluorometry. In the same rats the adenohypophyseal hormones as well as vasopressin, aldosterone (ALDO) and corticosterone (CORTICO) levels in serum were determined. Neuropeptide Y seems to induce a biphasic change in amine utilization in the tuberoinfundibular dopamine (DA) neurons and in the noradrenergic (NA) utilization in various hypothalamic areas. Thus, the lowest doses seem to inhibit the catecholamine utilization while higher doses seem to enhance it. NPY (250-750 pmol) reduced the serum levels of thyreotropine (TSH), prolactin (PRL) and growth hormone (GH) but increased CORTICO, adrenocorticotropin (ACTH) and ALDO serum levels. In conclusion, it is suggested that the NPY induced changes in DA utilization in the tuberoinfundibular DA neurons may contribute to the NPY induced changes in PRL and TSH secretion. The increases in paraventricular NA utilization may contribute to the increases in ACTH, ALDO and CORTICO secretion induced by NPY. These data give further support for NPY as an important neuroendocrine modulator.
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PMID:Further studies on the effects of central administration of neuropeptide Y on neuroendocrine function in the male rat: relationship to hypothalamic catecholamines. 358 2

Free water diuresis in vasopressin-deficient Brattleboro rats does not influence body conservation of chromium (Cr+3), suggesting a proximal tubular site for renal Cr reabsorption. Other data suggest that Cr conservation is accomplished primarily by lack of glomerular filtration or by tissue binding to a specific Cr-binding substance. To provide further data, radiochromium (51Cr) retention and tissue distribution were studied in SHR and WKY rats undergoing saline diuresis. Despite high urine flows, body retention and urinary excretion of 51Cr were unchanged. Tissue content of 51Cr was minimally and not consistently influenced by saline diuresis in either rat strain. Compared to WKY rats, the SHR rats had a trend to lower serum and tissue 51Cr content but higher tissue/serum 51Cr ratios. These data fail to incriminate collecting duct reabsorption in Cr conservation but are compatible with proximal Cr reabsorption or either of the two hypotheses mentioned above. The decreased serum 51Cr content of SHR rats may be due to the mechanical effect of increased plasma and extracellular volumes. One possible explanation for the increased tissue/serum 51Cr ratios may be the presence of a factor in SHR rats promoting cellular Cr transport. However, there is no present evidence to suggest that any of the hormones believed capable of increasing Cr transport (insulin, growth hormone, thyroxine, ADH) are increased in the SHR rat.
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PMID:Radiochromium distribution during saline diuresis. 373 75

Two adult patients with unilateral hypoplastic optic nerves, absent septa pellucida and hypopituitarism are described. Patient 1, aged 20, presented with diabetes insipidus due to partial vasopressin deficiency. Patients 2, aged 29, presented with focal epilepsy. Both had short stature. They showed absent growth hormone (GH) response to insulin-hypoglycaemia or glucagon, but responded to 100 micrograms growth hormone releasing factor (GRF-44) with a rise in circulating GH, suggesting a hypothalamic defect in GH release though a co-existing pituitary defect cannot be excluded. Other hypothalamic-pituitary functions were normal. These two patients probably represent the milder form of the clinical spectrum of septo-optic dysplasia which, with the extensive use of CT brain scans, will be increasingly encountered by physicians attending adult patients.
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PMID:Hypothalamic defects in two adult patients with septo-optic dysplasia. 375 51

To examine the influence of endogenous opioids on the hormonal response to isotonic exercise, eight males were studied 2 h after oral administration of placebo or 50 mg naltrexone, a long-lasting opioid antagonist. Venous blood samples were obtained before, during, and after 30 min of bicycle exercise at 70% VO2max. Naltrexone had no effect on resting cardiovascular, endocrine, or serum variables. During exercise epinephrine was higher [mean 433 +/- 100 (SE) pg/ml] at 30 min with naltrexone than during placebo (207 +/- 26 pg/ml, P less than 0.05). Plasma norepinephrine showed the same trend but the difference (2,012 +/- 340 pg/ml with naltrexone and 1,562 +/- 241 pg/ml with placebo) was not significant. Plasma glucose was higher at all times with naltrexone. However, the difference was significant only 10 min into recovery from exercise (104.7 +/- 4.7 vs. 94.5 +/- 2.8 mg/dl). Plasma growth hormone and cortisol increased during recovery and these elevations were significantly (P less than 0.05) augmented by naltrexone. Plasma vasopressin and prolactin increased with exercise as did heart rate, blood pressure, lactic acid, and several serum components; these increases were not affected by naltrexone. Psychological tension or anxiety was lower after exercise compared with before and this improved psychological state was not influenced by the naltrexone treatment. These data suggest that exercise-induced activation of the endogenous opioid system may serve to regulate the secretion of several important hormones (i.e., epinephrine) during and after exercise.
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PMID:Influence of endogenous opioids on the response of selected hormones to exercise in humans. 375 44

Lysine-8-vasopressin (LVP) for 10 days and in doses up to 13.5 LVP units did not significantly alter the Hamilton Depression Rating Scale scores of 12 severely depressed, treatment-resistant patients who were evaluated in a double-blind crossover study. The 24-h rhythms of melatonin, cortisol, growth hormone and prolactin appeared remarkably stable over the course of repeated measurement. LVP administration did not affect these 24-h rhythms.
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PMID:Effect of lysine vasopressin in depressed patients on mood and 24-hour rhythm of growth hormone, cortisol, melatonin and prolactin. 390 21


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