Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Using a specific radioimmunoassay for gamma-melanotropin (gamma-MSH), one of the predicted fragments in the amino-terminal portion of the adrenocorticotropin(ACTH)-beta-lipotropin (beta-LPH) precursor, gamma-MSH-like immunoreactivity (gamma-MSH-LI) was detected in human plasma from 4 of 5 patients with Addison's disease and 2 of 3 patients with Nelson's syndrome. None of the normal subjects or patients with Cushing's disease showed detectable concentrations (more than 150 pg/ml) of gamma-MSH-LI. gamma-MSH-LI was secreted concomitantly with ACTH-like immunoreactivity (ACTH-LI) and beta-endorphin-like immunoreactivity (beta-endorphin-LI) in response to insulin-induced hypoglycemia and the administration of lysine-vasopressin. Conversely, intravenous injection of cortisol lowered plasma concentrations of gamma-MSH-LI concomitantly with those of ACTH-LI and beta-endorphin-LI. Gel chromatographic studies of the plasma extracts showed a single peak of gamma-MSH-LI near the elution position of human beta-LPH. These results suggest that gamma-MSH-LI in human plasma is present as a big form and that this big gamma-MSH is secreted concomitantly with ACTH and beta-endorphin.
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PMID:Concomitant secretion of Y-MSH with ACTH and beta-endorphin in humans. 625 36

Basal and stimulated secretion of immunoreactive ACTH, LPH and beta-endorphin from four human pituitary tumours has been studied in vitro using a superfused, isolated cell system. Chromatography of cell secretions under acid-dissociating conditions demonstrated that the human tumor cells released immunoreactive peptides with the elution profiles of alpha h (1-39) ACTH, beta h-LPH, gamma h-LPH and beta h-endorphin confirming that beta h-endorphin is secreted by human pituitary tumour cells and is not formed by enzymic cleavage from beta h-LPH in blood. No alpha- or beta h-MSH, nor any higher molecular weight forms of ACTH or LPH were detected. The cells from all four tumours responded to stimulation with rat stalk-median eminence extract (SME) and synthetic AVP with a concomitant release of ACTH, beta-LPH, gamma-LPH and beta-endorphin. In contrast to the isolated rat anterior pituitary cells, the pattern of responses to SME and AVP were indistinguishable and the release provoked by rat SME could be accounted for virtually entirely by its vasopressin content. No stimulation of release was observed when the cells were exposed to a variety of biogenic amines. Addition of hydrocortisone to the perfusion buffer of two tumours resulted in a slow inhibition of both basal and stimulated ACTH and LPH release. These data demonstrate that human pituitary tumour tissue from patients with Cushing's disease and Nelson's syndrome can be studied in vitro and that such studies may contribute to a greater understanding of the aetiology of these diseases.
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PMID:Secretion of ACTH, LPH and beta-endophin from human pituitary tumours in vitro. 625 99

Tissue from histologically confirmed ACTH cell adenomas in Cushing's disease (CD) and Nelson's syndrome (NS) was gained by transsphenoidal surgery. Combined enzymatic and mechanic agitation of tumor tissue yielded a cell suspension. Aliquots of the cell suspension were transferred to superfusion chambers immediately after isolation and investigated for ACTH and beta-endorphin production. Feedback action of cortisol (CO) and dexamethasone on basal hormone production and on lysine vasopressin (LVP) induced ACTH secretion were studied. Adenomatous tissue and anterior lobe tissue from the same patient in CD could be investigated simultaneously in 4 cases. The paraadenomatous tissue showed depression of basal and LVP-induced ACTH secretion. In all adenomatous tissues investigated there was missing or reduced suppression of basal ACTH secretion by physiological levels of CO. CO not only failed to suppress LVP-induced ACTH secretion but also seemed to enhance LVP stimulation in some experiments. This study confirms former results, that a missing or inversed feedback action or glucocorticoids in adenoma cells is a mechanism involved in the pathological ACTH secretion in CD and NS. Bioassayable and immunoreactive ACTH from media of superfusion and short-term static incubation were compared with beta-endorphin and beta-LPH in an assay detecting these two peptides with equimolar sensitivity. Secretory patterns were basically parallel but great differences showed in quantities of hormones secreted. In addition, Sephadex G-50 gel chromatography was performed to separate beta-endorphin from beta-LPH and to calculate the ratios. These profiles show great variations between different adenomas.
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PMID:In vitro secretion of ACTH, beta-endorphin and beta-lipotropin in Cushing's disease and Nelson's syndrome. 626 13

ACTH excretion by cultured nonenzymatically dispersed pituitary tumor cells from a patient with Nelson's syndrome was studied. Hormone release was suppressed by 74 +/- 6% by the addition of 1 microM of the met-enkephalin analog FK 33824, while naloxone (1 microM) stimulated ACTH release by 70 +/- 5%. Somatostatin, dexamethasone, bromocriptine, and cyproheptadine in a concentration of 1 microM each inhibited ACTH release by 25 +/- 2%, 35 +/- 2%, 52 +/- 2%, and 61 +/- 4%, respectively, while lysine vasopressin (0.1 microM) and dibutyryl cAMP (5 mM) stimulated ACTH release by 112 +/- 8% and 220 +/- 4%, respectively. In conclusion, it was shown that the stimuli mentioned above directly affect ACTH secretion by the pituitary tumor cells. The inhibitory action of the met-enkephalin analog and the stimulatory action of naloxone on ACTH secretion make the presence of opiate receptors on this type of tumor likely.
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PMID:A met-enkephalin analog inhibits adrenocorticotropin secretion by cultured pituitary cells from a patient with Nelson's syndrome. 627 Jan 82

Cell suspensions of ACTH cell adenomas of 10 patients with Nelson's syndrome were investigated for in-vitro secretion of ACTH. Two incubation systems, one using incubation beakers and the other a superfusion system, were employed. The cells were tested for their reactivity to lysine-vasopressin (LVP), cortisol, and combinations of both. LVP regularly provoked a rapid significant increase of ACTH secretion. The effect of cortisol was heterogeneous. Paradoxical initial stimulatory effects of cortisol were observed. There was a suppressive effect in some patients, which correlates to low proliferative activity in histological evaluation. In both systems a low secretory activity coincided with high proliferative activity in vivo.
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PMID:In-vitro secretion of ACTH in Nelson's syndrome. 629 38

The effects of ovine CRF, lysine vasopressin (LVP), and their interrelationships, and rat hypothalamic extract (HME), on ACTH and beta-endorphin release by human pituitary tumor cells from two patients with Nelson's syndrome and one with Cushing's disease and on ACTH and cortisol secretion in vivo were studied. In cultured pituitary tumor cells, both LVP and CRF greatly stimulated ACTH and beta-endorphin release at maximally active concentrations of 0.1 microM and 10 nM, respectively. At these concentrations, the combination of the two substances had an additive or synergistic effect on hormone release. Low concentrations of HME potentiated and/or were synergistic with CRF-mediated ACTH release. In vivo, the combination of CRF (1 microgram/kg) and LVP (10 pressor units) induced greater ACTH release than the sum of the responses to CRF and LVP alone. This synergistic effect of CRF plus LVP concerned only ACTH release, while cortisol release after CRF plus LVP was equivalent to the sum of the maximal increments in this hormone after CRF and LVP alone. The peak levels of cortisol after a combination of CRF and LVP probably reflect the maximum stimulatory capacity of the adrenal cortex. These data support the concept that in man, both ovine CRF and vasopressin are corticotropin-releasing factors which act synergistically. Both substances might well regulate, at the pituitary level, the responsiveness of the pituitary-adrenal axis to stimuli reaching the hypothalamus. A test using ovine CRF and LVP together might provide a better index of total pituitary ACTH reserve than one using the two compounds separately.
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PMID:Corticotropin-releasing factor (ovine) and vasopressin exert a synergistic effect on adrenocorticotropin release in man. 631 46

Opioid peptides are found throughout the central nervous system, and have profound effects on neuroendocrine function. In man, exogenous opiates and opioids elevate circulating prolactin, GH and TSH, and suppress the release of the gonadotrophins and pro-opiocortin-related peptides. However, unlike in other species, there is substantial evidence for a physiological role of endogenous opioids only in the case of the gonadotrophins and ACTH/LPH. Most evidence suggests that LH and FSH are modulated via the hypothalamus or amygdala, where concentrations of opioids and opioid receptors are very high. Endogenous opioids appear to be principally concerned with the frequency-modulated release of GnRH, and this may be important clinically in patients presenting with amenorrhoea. ACTH/LPH are under tonic inhibition by endogenous opioids acting at hypothalamic and/or pituitary levels, and changes in this inhibition may be responsible for the release of these peptides in response to certain forms of stress. It has been reported that the opiate antagonist, naloxone, is clinically useful in paradoxically inhibiting the release of ACTH in patients with Nelson's syndrome, but this requires adequate confirmation. Vasopressin is under biphasic opiate control, but the principal effect is probably opiate-mediated inhibition of vasopressin release. The endogenous ligand for this response is likely to be dynorphin. Suppression of vasopressin release by opiates may become a useful therapy in the treatment of the 'Syndrome of inappropriate ADH'.
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PMID:Brain opiates and neuroendocrine function. 632 67

Dispersed corticotrophic cells of 3 patients with Nelson's syndrome were studied in tissue culture for up to 25 days. During this culture period a parallel decrease with time was seen in ACTH and beta-endorphin-like immunoreactivity ( LIR ) release. A concomitant decline was observed for intracellular hormones. The time course of hormone release showed a parallel secretion of ACTH and beta-endorphin- LIR up to 8 h. Both the release of ACTH and beta-endorphin LIR were stimulated by 0.1 microM lysine vasopressin (LVP) in all three adenoma cell cultures. Dexamethasone (0.1 and 1 microM) suppressed basal hormone secretion for 4 h. Synthetic ovine corticotrophin-releasing factor (CRF) at 10 and 100 nM stimulated the secretion of ACTH and beta-endorphin LIR maximally. This stimulation was higher than observed with maximal stimulative concentration of LVP (0.3 microM). The CRF-mediated hormone secretion was calcium-dependent. Dexamethasone (0.1 microM) blocked the stimulating effect of 10 nM CRF completely. Gel-filtration chromatography demonstrated the cells to secrete both beta-lipotrophin (beta-LPH) and beta-endorphin. The ratio of beta-LPH to beta-endorphin released remained constant upon stimulation by LVP and CRF. HPLC studies demonstrate the possibility that several beta-endorphin fragments, including alpha-endorphin and gamma-endorphin, were secreted by cells from a Nelson tumour. CRF caused a simultaneous parallel stimulation of the release of these peptides.
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PMID:ACTH and beta-endorphin secretion by three corticotrophic adenomas in culture. Effects of culture time, dexamethasone, vasopressin and synthetic corticotrophin releasing factor. 632 19

Radioimmunoassay of methionine-enkephalin, leucine-enkephalin and beta-endorphin were used in order to study the distribution and release of endorphins. The distribution pattern of enkephalin immunoreactivity in brain, including human brain, is quite different from that of beta-endorphin immunoreactivity. Separation of beta-endorphin and beta-lipotropin by column chromatography revealed that the contribution of beta-lipotropin to beta-endorphin immunoreactivity in brain is very small. In the anterior lobe of the pituitary both beta-endorphin and beta-lipotropin were found, whereas in the intermediate/posterior lobe almost all immunoreactivity was due to beta-endorphin; considerable amounts of enkephalin were also detected. Raising the concentration of potassium ions stimulated the release of met- and leu-enkephalin from striatal slices and the release of beta-endorphin immunoreactive material(s) from hypothalamic slices; both phenomena were dependent upon the presence of calcium ions. Studies of the release of beta-endorphin from isolated rat pituitaries revealed characteristic differences between the anterior and intermediate/posterior lobes; e.g., lysine vasopressin and extracts from the median eminence were highly effective in releasing beta-endorphin from the anterior lobe without affecting the release from the intermediate/posterior lobe; on the other hand, dopamine inhibited beta-endorphin release from the intermediate/posterior lobe without affecting release from the anterior lobe. Increased beta-endorphin levels were found after various stress conditions in rat plasma, as well as after treatment with metyrapone and vasopressin. In normal human plasma significant amounts of beta-endorphin were detected; increased levels were found in Addison's, Nelson's and Cushing's disease. Chronic opiate treatment of rats for 10 days did not affect brain levels of enkephalin or the beta-endorphin content of the hypothalamus, pituitary and plasma. Precipitated withdrawal decreased beta-endorphin in the anterior lobe and hypothalamus and increased beta-endorphin levels in the plasma. Long-term morphine treatment (30 days) decreased enkephalin and beta-endorphin content in some brain areas and in the intermediate/posterior pituitary lobe but not in the anterior lobe.
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PMID:Functional aspects of endorphins. 744 28

Furosemide attenuates airway obstruction in asthmatic subjects when administered as an aerosol pretreatment. This protective effect of furosemide could be related to relaxation of bronchial smooth muscle or to increased bronchial blood flow. To determine whether furosemide dilates bronchial smooth muscle, isometric contractile responses in distal bronchi from young pigs were studied. In bronchial smooth muscle rings that were precontracted with 10(-5) M acetylcholine, significant relaxation occurred with 10(-8) to 3 x 10(-6) M isoproterenol but not with 10(-8) to 10(-3) M furosemide. In contrast, bronchial arteries that were precontracted with either 10(-4) M norepinephrine or 10(-8) M vasopressin significantly relaxed in response to 10(-4) to 3 x 10(-3) M and 10(-3) to 3 x 10(-3) M furosemide, respectively. We conclude that furosemide, under the described experimental conditions, relaxes airway vascular smooth muscle but not bronchial smooth muscle. These results are consistent with previous suggestions that inhaled furosemide increases blood flow to airway tissues (Gilbert IA, Lenner KA, Nelson JA, Wolin AD, and Fouke JM. J Appl Physiol 76: 409-415, 1994).
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PMID:Differential effects of furosemide on porcine bronchial arterial and airway smooth muscle. 1100 70


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