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)

Properties of adenyl cyclase of normal adrenals and of a corticosterone-producing adrenal cancer of the rat have been compared. Enzyme activity was found in all particulate fractions of both tissues. The cyclase of the tumor as well as of the adrenals was stimulated by adrenocorticotropic hormone (ACTH) over similar concentration ranges. Unexpectedly, the tumor enzyme was also stimulated by epinephrine, norepinephrine, and thyroid-stimulating hormone (TSH). These hormones produced a dose-related effect over a concentration span that was comparable with that for ACTH. The tumor cyclase was not responsive to angiotensin Il, vasopressin, glucagon, insulin, growth hormone, parathyroid hormone, and thyrocalcitonin. ACTH was the only hormonal preparation that stimulated normal adrenal cyclase. These findings are compatible either with the possibility that the adenyl cyclase receptor of the tumor has undergone structural alteration with a consequent loss of specificity for ACTH or with the possibility that the tumor possesses several cyclase regulatory receptors.
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PMID:Abnormal hormone responses of an adrenocortical cancer adenyl cyclase. 432 11

Protein carboxymethylase, an enzyme capable of methylating proteins and polypeptides, was purified from bovine pituitary. The anterior pituitary hormones, luteinizing hormone, follicle-stimulating hormone, adrenocorticotropic hormone, growth hormone, thyroid-stimulating hormone, and prolactin, were found to be substrates for this enzyme. The posterior pituitary hormones, oxytocin and vasopressin, did not serve as substrates. With luteinizing hormone as the substrate, protein carboxymethylase had a pH optimum near pH 5.5. A limiting K(m) of 1.47 muM for S-adenosyl-L-methionine was obtained with luteinizing hormone as the methyl acceptor. Possible roles of this enzyme in the posterior and anterior pituitary are discussed.
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PMID:Characterization and substrate specificity of a protein carboxymethylase in the pituitary gland. 436 60

A 29-year-old woman with evidence of a craniopharyngioma and documented panhypopituitarism is described. Clinical and laboratory evaluation revealed deficiencies of follicle-stimulating hormone, luteinizing hormone, thyroid-stimulating hormone, growth hormone, prolactin, adrenocorticotropic hormone and antidiuretic hormone. Prompt release of several pituitary hormones was noticed after administration of the hypothalamic releasing hormones FSH/LH-RF and thyrotropin-releasing hormone, whereas insulin-induced hypoglycemia, levodopa, chlorpromazine and clomiphene citrate, all of which act at the level of the hypothalamus, did not alter basal pituitary secretion. The patient's height of 60 inches, despite panhypopituitarism, and the interpretation of the above data are discussed in the light of current concepts regarding the dynamics of the hypothalamic-hypophyseal system.
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PMID:Survival and growth in a woman with untreated hypothalamic panhypopituitarism of 21 years' duration. 437 Apr 18

An assay for the binding of [(3)H]thyrotropin-releasing hormone ([(3)H]TRH) is described. Plasma membranes isolated from bovine anterior pituitary gland bind about 600 femtomoles of this hormone per mg of protein, as compared to 15 femtomoles per mg of protein in the total adenohypophyseal homogenate (40-fold purification). The equilibrium constant of membrane receptor-[(3)H]TRH binding at 0 degrees C is 4.3 x 10(7) L.M(-1), or a half-maximal binding of this hormone at 23 nM. The binding is time-dependent; addition of unlabeled hormone induces dissociation of the receptor-[(3)H]TRH complex with a half-life of 14 min. The binding of TRH is not altered by 10 muM melanocyte-stimulating hormone-release inhibiting hormone, lysine-vasopressin, adrenocorticotropin, growth hormone, prolactin, luteinizing hormone, insulin, glucagon, L-thyroxine, or L-triiodothyronine. K(+) and Mg(++) increase formation of the receptor-TRH complex at optimal concentrations of 5-25 mM and 0.5-2.5 mM, respectively, with inhibition at higher concentrations. Ca(++) inhibits binding of TRH at all concentrations tested.
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PMID:Binding of thyrotropin-releasing hormone to plasma membranes of bovine anterior pituitary gland (hormone receptor-adenylate cyclase-equilibrium constant-( 3 H)thyrotropin). 462 48

Peptide hormones labelled with radioactive iodine were partitioned into the aqueous two-phase polymer systems developed by Albertsson (1960) and the conditions required for separation of free from antibody-bound hormone have been worked out. Hormones studied included insulin, growth hormone, parathyroid hormone and [arginine]-vasopressin. Free and antibody-bound hormones show different distribution coefficients in a number of systems tested; two systems, the dextran-polyethylene glycol and dextran sulphate-polyethylene glycol system, give optimum separation. Free hormones distribute readily into the upper phase of these systems, whereas hormone-antibody complexes, as well as uncombined antibody, are found almost completely in the lower phase. Various factors including the polymer concentration, the ionic composition of the system, the nature of the hormone and the nature of added serum protein differentially affect the distribution coefficients for free and antibody-bound hormone. These factors can be adequately controlled so as to improve separation. The two-phase partition method has been successfully applied to measure binding of labelled hormone to antibody under standard radioimmunoassay conditions. It exhibits several advantages over the method of equilibration dialysis and can be applied to the study of non-immunological interactions.
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PMID:Distribution of free and antibody-bound peptide hormones in two-phase aqueous polymer systems. 467 74

The endogenous opiate system is involved in the regulation of numerous bodily functions, but the literature suggests that the effects of endogenous opioids differ among species and between animals and man. Naltrexone, a relatively pure opiate antagonist, appears to have significant effects on the secretion of the gonadotropins (luteinizing hormone and follicle-stimulating hormone), adrenocorticotropin (ACTH), cortisol, and probably catecholamines. Naltrexone appears to have minor or no effects on prolactin, the pituitary-thyroid axis, growth hormone, insulin, glucagon, vasopressin, and the gut hormones. Naltrexone also seems to reduce food intake and cause weight loss in humans. The dosages of opiate antagonist and the presence of other variables play a major role in the responses seen in various studies.
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PMID:Endocrine and metabolic effects of opiate antagonists. 608 67

Somatostatin receptors in the rat pituitary gland were characterized by binding analysis with a radioiodinated high affinity somatostatin analogue, 125I-Tyr1[D-Trp8]somatostatin. Receptor binding of this derivative reached equilibrium at 30 min and was maintained at a plateau for at least 60 min. Two L-Trp8- labeled somatostatin analogues. 125I-Tyr1- and [125I-Tyr11]somatostatin, displayed less stable and lower specific uptake and higher nonspecific binding. In contrast to the rapid degradation of the L-Trp8 ligands during binding assay, 125I-Tyr1]D-Trp8]somatostatin retained more than 80% of its binding activity after 90 min of incubation with pituitary particles. Pituitary particles bound 125I-Tyr1]D-Tyr8]somatostatin with high affinity (Ka = 8.6 +/- 1.2 X 10(9) M-1) and capacity of 54.4 +/- 2.6 fmol/mg. These binding sites showed specificity for the native peptide and its active analogues, and other peptide hormones, including angiotensin II, thyrotropin-releasing hormone, vasopressin, oxytocin, substance P, and gonadotropin-releasing hormone, did not inhibit tracer binding. A good correlation was observed between the binding affinities of several somatostatin analogues and their potencies as inhibitors of growth hormone release in rat pituitary cells. These findings emphasize the physiological importance of the pituitary somatostatin receptor in mediating the inhibitory action of the peptide on growth hormone release. The use of Tyr1[d-Trp8]somatostatin as a labeled ligand permits accurate determinations of the binding affinity and concentration of receptors for somatostatin in the normal pituitary gland and provides a basis for further studies of somatostatin receptor regulation and receptor-mediated cellular effects of the tetradecapeptide.
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PMID:Pituitary somatostatin receptors. Characterization by binding with a nondegradable peptide analogue. 612 Jan 62

We have previously reported that maternal deprivation of rat pups causes a decrease in tissue responsiveness to growth hormone that is mediated by the loss of maternal tactile stimulation. We now report that liver responses to alpha and beta adrenergic agonists as well as glucagon and vasopressin decrease during maternal deprivation. However, the decreased responsiveness to these agents is mediated by short-term food deprivation (FD) rather than loss of maternal tactile stimulation. When 8-day-old rat pups were separated from the mother or placed with a nipple-ligated mother for 2 hr and then injected with phenylephrine, isoproterenol or glucagon, liver ornithine decarboxylase (ODC) activity did not increase, although ODC activity increased markedly in control pups after administration of these agents. This loss of responsiveness appears to be both tissue- and drug-specific, as liver ODC responses to dexamethasone, dibutyryl cyclic AMP and prostaglandin E-1 and heart ODC responses to phenylephrine were not affected. FD had only a slight effect on glycogen phosphorylase activation by phenylephrine and had no effect on phenylephrine-induced glycogen depletion. Finally, FD did not affect the number of alpha-1 or beta receptors in liver of rat pups. These findings suggest that short-term FD selectively decreases liver ODC responses to certain agonists including alpha and beta adrenergic agonists by postreceptor mechanisms.
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PMID:Selective loss of ornithine decarboxylase response to adrenergic agonists and glucagon during food deprivation of neonatal rats. 613

We studied the hormonal responses to a generalized tonic-clonic convulsion in 20 patients with idiopathic or posttraumatic epilepsy (6 patients) or alcohol-withdrawal seizures (14 patients). We found an increase shortly after the seizure in plasma levels of ACTH, beta endorphin, beta lipotropin, prolactin, and vasopressin, and a later increase in plasma cortisol. There was no significant change in levels of growth hormone, luteinizing hormone, follicular stimulating hormone, or plasma renin activity. An increase in plasma ACTH level was accompanied by a rise in beta lipotropin and beta endorphin, and followed by a rise in plasma cortisol. In 2 patients there was no postictal increase in plasma prolactin, despite changes in other hormones. There was no difference in the nature or time course of the hormonal changes in patients with alcohol-withdrawal seizures and those with seizures from other causes. The mechanisms subserving these changes are unknown. Nonspecific stress influences the release of certain hormones, but the absence of a significant growth hormone response suggests that this was probably not responsible for our findings. It is possible that the generalized neuronal discharge of a seizure stimulates the hypothalamus either directly, through specific neurotransmitter changes, or through the release of other substances. One possibility that we are investigating in experimental animals is that endogenous opioids are involved, especially in the release of prolactin.
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PMID:The hormonal responses to generalized tonic-clonic seizures. 614 54

In general, the endogenous opioid peptides (EOP), morphine (MOR), and related drugs exert similar effects on acute release of pituitary hormones. Thus administration of opiates produces a rapid increase in release of prolactin (PRL), growth hormone (GH), adrenocorticotropin (ACTH), and antidiuretic hormone (ADH), and a decrease in release of gonadotropins and thyrotropin (TSH). Although not yet fully established, there is growing evidence that the EOP participate in the physiological regulation of pituitary hormone secretion. Thus naloxone (NAL), a specific opiate antagonist, has been shown to reduce basal serum levels of PRL and GH, and to elevate serum levels of LH and follicle stimulating hormone in male rats. Other reports have shown that NAL can inhibit the stress-induced rise in serum PRL, raise the castration-induced increase in serum LH to greater than normal castrate values, and counteract the inhibitory effects of estrogen and testosterone on LH secretion. Opiates appear to have no direct action on the pituitary, but there is evidence that they can alter activity of hypothalamic dopamine and serotonin in modulating secretion of pituitary hormones.
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PMID:Influence of endogenous opiates on anterior pituitary function. 624 13


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