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

Based on drug release by microporous hollow fibers and the recent introduction of microporous polymers, a new technique was developed for controlled delivery of peptides. Small-diameter microporous polypropylene tubing, lumen-loaded with microgram quantities of vasopressin, and coated with collodion, releases vasopressin after in vitro immersion slowly (1-100 ng/d) and constantly for months. The mechanism of pseudo-zero-order delivery is based on high adsorption of vasopressin, keeping the void volume concentration of dissolved vasopressin constant, which is consequently a constant driving force of outward diffusion. The collodion coating prevents the entry of proteinaceous compounds which would result in rapid desorption of vasopressin. The present delivery module provides a lasting release for other peptides as well (lysine-vasopressin, oxytocin, alpha-melanocyte-stimulating hormone and, to a lesser extent, Met-enkephalin). The microporous polymer-collodion device is biocompatible and, loaded with vasopressin, successfully alleviates the diabetes insipidus of Brattleboro rats deficient for vasopressin. Subcutaneous implantation normalized diuresis for a period of 60 d and constant urine vasopressin excretion is observed. When the commercially available osmotic minipump is too large for implantation, the small size of the present controlled-delivery system allows peptide treatment of young and immature laboratory rats, even if located in utero.
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PMID:Controlled long-term release of small peptide hormones using a new microporous polypropylene polymer: its application for vasopressin in the Brattleboro rat and potential perinatal use. 652 41

The Brattleboro rat carries as a recessive trait the inability to synthesize hypothalamic vasopressin and its related neurophysin but is able to synthesize oxytocin and its neurophysin. Brattleboro rats homozygous for this trait have no immunologically detectable circulating vasopressin and manifest a complete syndrome of diabetes insipidus, which is corrected with vasopressin replacement therapy. Such a defect could be due to absence of the gene encoding vasopressin, the presence of an abnormal gene, or a variety of transcriptional or posttranscriptional abnormalities. We report here that the hypothalamus of the Brattleboro rat contains detectable, although markedly reduced, levels of an mRNA indistinguishable in size with and similar in sequence to authentic vasopressin mRNA. Corresponding levels of oxytocin mRNA were the same in Brattleboro and normal rat hypothalami. These findings indicate that the Brattleboro rat expresses a vasopressin gene, but at a reduced level.
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PMID:Vasopressin gene is expressed at low levels in the hypothalamus of the Brattleboro rat. 659 Nov 92

The localization of CRF-41 related peptide was studied in the brain and posterior pituitary of the homozygous rats for the inherited diabetes insipidus (Brattleboro strain, DI) and of the Long-Evans rats (LE) as control. It was compared to the distribution of vasopressin (AVP), oxytocin (OXY) and OXY-neurophysin (N I). In both strains, CRF-41 was identified in two morphologically distinct systems: one was a hypothalamoneurohypophysial system simultaneously containing CRF-41, OXY and N I; the other was a hypothalamoinfundibular system carrying CRF-41 only. CRF containing neurons were located in the periventricular area of the anterior hypothalamus, in the retrochiasmatic part of the supraoptic nuclei (SON) and, for some of them, in the antechiasmatic part of SON. CRF immunostainings were enhanced by colchicine treatment in LE rats and by DDAVP therapy in DI rats.
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PMID:Comparative immunocytochemical localization of corticotropin releasing factor (CRF-41) and neurohypophysial peptides in the brain of Brattleboro and Long-Evans rats. 660 39

Five members of a family with dominantly inherited diabetes insipidus were diagnosed and treated with deamino-d-arginine vasopressin (DDAVP), a vasopressin analogue given intranasally. All subjects demonstrated subnormal levels of arginine vasopressin (AVP) by radioimmunoassay in response to cigarette smoke inhalation, a standardized nicotine stimulation test. Levels of oxytocin (OT) were found to be normal and unstimulated after cigarette inhalation in two subjects, but when two affected male siblings ingested Ovulen, OT and ESN were stimulated to subnormal levels. After twelve months of DDAVP treatment, the low AVP response to nicotine was preserved whereas the carrier protein, nicotine stimulated neurophysin (NSN) remained undetectable.
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PMID:Familial central diabetes insipidus: vasopressin and nicotine stimulated neurophysin deficiency with subnormal oxytocin and estrogen stimulated neurophysin. 663 59

The cardiovascular effects of intravenous and intracisternal administration of neurohypophysial peptides were studied in anaesthetized dogs. Intracisternal oxytocin (1 and 10 mU kg-1) increased blood pressure. Intravenous lysine vasopressin (0.1 to 100 mU kg-1) induced a dose-dependent increase in blood pressure with bradycardia. Intracisternal lysine vasopressin (0.01 to 10 mU kg-1) elicited a dose-related decrease in blood pressure but no change in heart rate. These central hypotensive effects of vasopressin were suppressed by intravenous guanethidine, dl-propranolol, prazosin or atropine and were not observed in diabetes insipidus dogs with surgical lesion of the supra-opticohypophysial tract. Hypotension elicited by intracisternal vasopressin was due to a decrease in sympathetic tone and simultaneous activation of parasympathetic tone. These results suggest the involvement of these peptides in central control of blood pressure.
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PMID:Neurohypophysial peptides and central cardiovascular control. 666 21

Plasma concentrations of oxytocin and vasopressin were determined by radioimmunoassay in a woman with clinical diabetes insipidus. Plasma oxytocin levels were normal and ranged from less than 0.25 microU/ml to 76 microU/ml during the last month of pregnancy and during spontaneous labor. Vasopressin requirements did not change during pregnancy. Unexplained vasopressin resistance and massive diuresis occurred early in the postpartum period. Plasma vasopressin concentrations were undetectable in the nonpregnant state. The documentation of normal oxytocin production and total vasopressin deficiency suggests that an anatomic defect is unlikely to cause this disorder unless it is limited to axons and cell bodies containing vasopressin and not oxytocin.
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PMID:Plasma oxytocin concentrations in a pregnant woman with total vasopressin deficiency. 683 22

The activity of protein carboxymethylase and the endogenous protein methyl acceptor capacity were examined in the posterior, intermediate, and anterior lobes of the pituitaries of homozygous Brattleboro rats with diabetes insipidus and in heterozygous Brattleboro and Long-Evans control rats. Protein carboxyl methylation is selectively altered in the posterior pituitary lobes of homozygous Brattleboro rats. Protein carboxymethylase activity is higher (+40%) and endogenous methyl acceptor protein capacity is lower (-80%) with respect to heterozygous Brattleboro and Long-Evans control rats. This latter change is correlated with decreased methylation of proteins of a molecular weight of approximately 11K daltons, is selective for the posterior pituitary lobe, since it does not occur in the intermediate and anterior lobes, and probably reflects the absence of vasopressin-associated neurophysin in homozygous Brattleboro rats. Our results support a physiological role of protein carboxyl methylation in the neurosecretory process in the posterior pituitary gland.
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PMID:High-protein carboxymethylase activity and low endogenous methyl acceptor proteins in posterior pituitary lobe of rats lacking neurophysin-vasopressin (Brattleboro rats). 686 19

1. By immunoperoxidase technique, immunoreactive angiotensin II (ANG II) was located in the cell bodies of many magnocellular neurons in the supraoptic and paraventricular nuclei of the hypothalamus and their pathways to median eminence and posterior pituitary gland in the rat. 2. Like vasopressin and its neurophysin, but not oxytocin, ANG II was also found in parvocellular neurons in the suprachiasmatic nucleus. 3. Analysis of these peptides in the same magnocellular neurons reveals that ANG II is localized primarily in vasopressin cells. 4. Like vasopressin and its precursor, ANG II is deficient in homozygous Brattleboro rats with diabetes insipidus. 5. In adrenalectomized rats increases in vasopressin and its neurophysin in median eminence are associated with increases in ANG II. 6. The data suggest that the ANG II demonstrated shares antigenic determinants with the vasopressin precursor, or is regulated in a similar way to vasopressin in the same neurons.
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PMID:Immunocytochemical localization of angiotensin II and vasopressin in rat hypothalamus: evidence for production in the same neuron. 700 38

A cell-by-cell analysis of the magnocellular elements in hypothalami of fifty Long-Evans (normal) and Brattleboro (diabetes insipidus) rats was done using the unlabeled antibody enzyme technique (PAP) with primary antisera directed against oxytocin (OXY), vasopressin (ADH), and the neurophysins. The magnocellular neurons of the hypothalamus were found in the supraoptic (SON), paraventricular (PVN), and anterior commissural (ACN) nuclei, a number of accessory nuclei, and as individual cells in the anterior hypothalamic area. SON was divided by the optic tract into the principal part and retrochiasmatic SON. In retrochiasmatic SON a majority of the cells contained vasopressin. Within the principal part of SON oxytocin-producing cells tended to be found rostrally and dorsally, while the vasopressin cells were more common caudally and ventrally. PVN was divided into three subnuclei, the medial, lateral, and posterior subnuclei, on the basis of cellular morphology and peptide content. The magnocellular cells of the medial and lateral PVN were closely packed together and nearly round, while those of posterior PVN were more separated and fusiform in shape with their long axis running in a medio-lateral direction. Medial PVN consisted primarily of oxytocin-producing cells, while lateral PVN was formed by a core of vasopressin-producing cells with a rim of oxytocin cells. Posterior PVN contained largely oxytocin-producing cells. Both ADH and OXY cells were found in the accessory nuclei. In the Long-Evans rat the SON had, on the average, 1443 OXY and 3236 ADH cells; the PVN had 1174 OXY and 976 ADH cells; and the accessory magnocellular groups in the hypothalamus (including the ACN) had 1286 OXY and 552 ADH cells. The Brattleboro strain animal had similar numbers of cells in these nuclei. (The cells which contain ADH in normal animals were identified in the Brattleboro rat as large, neurophysin-negative cells.) Thus, a large fraction of the magnocellular oxytocin- and vasopressin-producing cells in the rat were located outside of the PVN and SON. One accessory cell group in particular, ACN, had 616 OXY cells, or about 50% as many as PVN. In each nucleus the sum of the numbers of OXY and ADH cells was approximately the number of neurophysin cells.
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PMID:Immunohistochemical analysis of magnocellular elements in rat hypothalamus: distribution and numbers of cells containing neurophysin, oxytocin, and vasopressin. 701 60

The binding of [3H]corticosterone to receptors in cytosol of several brain regions and of [3H]dexamethasone to receptors in pituitary cytosol was measured after chronic treatment of homozygous diabetes insipidus rats (Ho-Di) with various neuropeptides. All rats were adrenalectomized 24 h before sacrifice for depletion of endogenous adrenal hormones and at that time administration of the peptides was discontinued. At sacrifice the rats were perfused with saline to remove plasma transcortin from the tissues. The apparent maximal binding capacity for corticosterone and dexamethasone was significantly lower in hippocampus and anterior pituitary (36.8% and 39.2%, respectively) of Ho-Di rats than of homozygous nondiabetic rats (Ho-No) of the same strain. In contrast, the neurointermediate pituitary lobe of Ho-Di rats had more than twice as many (211%) binding sites, whereas neither receptor capacity in hypothalamus and septum nor plasma transcortin in these rats were significantly different from those in Ho-No rats. Treatment of Ho-Di rats with arginine-vasopressin, des-glycinamide arginine vasopressin, or 1-desamino-8-D-arginine-vasopressin daily for 1 week resulted in an elevation of receptor capacity in hippocampus and anterior pituitary near the level observed in nondiabetic controls. No effects on the other brain regions, the neurointermediate pituitary lobe, and on plasma transcortin were observed with these peptide treatments. Administration of oxytocin and ACTH-(4-10) did not affect receptor binding. It is concluded that in the Ho-Di Brattleboro rat the glucocorticoid receptor system in the hippocampus and in the anterior pituitary is selectively affected by neuropeptides related to vasopressin.
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PMID:Vasopressin-related peptides increase the hippocampal corticosterone receptor capacity of diabetes insipidus (Brattleboro) rats. 705 79


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