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)

Carboxypeptidase H is one of several enzymes required for the processing of peptide hormone precursors. In this study, inhibition of carboxypeptidase H by its peptide products was investigated. Carboxypeptidase H activity in bovine adrenal medulla chromaffin granules and rat adrenal medulla homogenate was inhibited by the peptides Met- and Leu-enkephalin, vasopressin, oxytocin, luteinizing hormone-releasing hormone, substance P, and thyrotropin-releasing hormone, with oxytocin and ACTH 1-14 having the least effect, at concentrations of 2-20 mM. Inhibition by amidated peptide products (vasopressin, oxytocin, luteinizing hormone-releasing hormone, substance P, and thyrotropin-releasing hormone) show that the final products of the precursor processing pathway can regulate carboxypeptidase H. These levels of peptides are similar to known intragranular peptide concentrations indicating that product and feedback inhibition of carboxypeptidase H may play a role in the control of neuropeptide synthesis. The proenkephalin-derived peptides Met-enkephalin, Leu-enkephalin, Met-enkephalin-Arg6-Gly7-Leu8, and Met-enkephalin-Arg6-Phe7 competitively inhibited bovine and rat carboxypeptidase H with Ki values of 12.0, 6.5, 7.0, and 5.5 mM, respectively. The significantly greater Ki for Met-enkephalin may reflect the effects of higher intragranular concentration of Met-enkephalin, since one proenkephalin molecule contains four copies of Met-enkephalin and only one copy of each of the other enkephalin peptides. Thus, the products from one multivalent precursor molecule may equivalently inhibit carboxypeptidase H activity. Product inhibition of carboxypeptidase H and perhaps other processing enzymes may serve to limit the maximum peptide concentration within the secretory vesicle.
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PMID:Product inhibition of carboxypeptidase H. 288 69

Agonist-induced accumulation of [3H]inositol-1-phosphate ([3H]IP1) was studied using human embryonic pituitary tumour cells (Flow 9000). Stimulation of Flow 9000 cells, prelabelled with [3H]inositol, with the nonapeptide bradykinin (BK), or its analogues and fragments produced a differential accumulation of [3H]IP1. BK-related peptides exhibited the following rank order of potency in this assay: BK = [Lys]BK greater than [Met-Lys]Bk much greater than [Des-Arg9]BK much greater than BK(1-6) = BK(2-7) = BK(2-9). BK and [Lys]BK produced half-maximal effects at 2-3 nM. [3H]BK receptor binding studies showed that BK and [Des-Arg9]BK produced a concentration-dependent inhibition of [3H]BK binding with Ki values of 4.8 +/- 1.9 nM (n = 3) and 6.8 +/- 0.7 microM (n = 3) respectively. These studies suggest the presence of B2-bradykinin receptors on the human embryonic pituitary tumour cell-line which appear to be coupled to the phosphatidyl inositol turnover signal transduction mechanism. Cholecystokinin, angiotensin II, vasopressin, thyrotropin-releasing hormone and bombesin also stimulated [3H]IP1 production but were generally much weaker than BK. In contrast, substance P, eledoisin, somatostatin, neurotensin, VIP, NPY, CGRP, U50488, DAGO and DADLE appeared inactive in this system at 10 microM.
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PMID:Bradykinin-induced accumulation of [3H]inositol-1-phosphate in human embryonic pituitary tumour cells by activation of a B2-receptor. 289 11

1. The changes in FMRFamide (Phe-Met-Arg-Phe-NH2) immunoreactivity in response to incubation in dopamine, serotonin, met-enkephalin, oxytocin, arg-vasopressin and FMRFamide were examined in the central nervous system of the snail, Achatina fulica. 2. When the central nervous system was cultured in medium which contained dopamine and in medium which contained serotonin, the number of immunoreactive neurons increased in the anterior part of the cerebral ganglion and decreased in the sub-esophageal ganglion. 3. When arg-vasopressin was added to the culture medium, the number of immunoreactive neurons increased in the pedal ganglion and decreased in the other sub-esophageal ganglion. 4. By contrast, when the central nervous system was cultured in medium which contained oxytocin, the number of immunoreactive neurons did not increase, but rather decreased, in each ganglion. 5. No changes in immunoreactivity were detected in the central nervous system when it was cultured in medium which contained FMRFamide. 6. It appears, from these results, that the production and release of FMRFamide from different neurons are differentially affected by the physiologically active substances tested.
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PMID:Dynamics of FMRFamide immunoreactivity in response to physiologically active substances in the central nervous system of the snail, Achatina fulica. 290 40

The effect of two analogues of [Met]-enkephalin, [D-Ala2,N-Phe4,Met(0)-ol5]-enkephalin and its guanyl derivative, on plasma concentrations of atrial natriuretic peptide (ANP) and serum aldosterone in six normal subjects was investigated. All subjects were given a 1 litre water load to inhibit vasopressin release. Both analogues, when injected i.v. at a dose of 100 micrograms, stimulated release of prolactin and GH and inhibited serum cortisol; there was no significant change in blood pressure, pulse rate or urine output. Neither plasma concentrations of ANP nor serum aldosterone levels changed significantly after injection of either analogue at a low or high dose. Naloxone, given i.v. as an 8 mg bolus, also failed to alter concentrations of either ANP or aldosterone, while it significantly stimulated the release of serum LH and cortisol. It was concluded that under basal conditions opiate receptors are unable to modulate plasma ANP or serum aldosterone concentrations.
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PMID:Opioid peptides do not modulate atrial natriuretic peptide or aldosterone release under basal conditions in man. 296 6

Enkephalins are found in the posterior pituitary, can alter vasopressin secretion, and have greater pressor effects in spontaneously hypertensive rats (SHR) than in Wistar-Kyoto (WKY) rats. Measurement of the plasma methionine-enkephalin concentration (PMet-Enk) has provided equivocal results in humans and has not been reported in rats. We have developed a highly specific and sensitive Met-Enk radioimmunoassay and determined that Met-Enk circulates in rats but that PMet-Enk is no different between SHR and WKY rats (7.6 +/- 0.8 and 9.2 +/- 0.8 pg/ml, respectively). Water deprivation for 48 h increased the plasma vasopressin concentration (PADH) and 24-h urinary vasopressin excretion (UADHV) in SHR and WKY rats, but PMet-Enk was not altered. There were no differences in PADH and UADHV between SHR and WKY rats in either the euhydrated or dehydrated state. These results suggest that it is unlikely that circulating Met-Enk contributes importantly to the maintenance of hypertension in SHR. There was also no evidence for a greater secretion of vasopressin in SHR than in WKY rats, in contrast to previous reports.
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PMID:Methionine-enkephalin and vasopressin in SHR: effects of dehydration. 371 73

Renal cortical necrosis was induced by the administration of vasopressin to oestrogen-pretreated rats. Histochemical (succinic dehydrogenase, trichrome, perjod acid Schiff) and electronmicroscopic methods were applied to examine how the vasopressin antagonist d(CH2)5Tyr(Met)AVP influences the development of this renal cortical necrosis. The experiments revealed that vasopressin did not induce hypoxia or necrosis in the renal tubules if the antagonist was administered simultaneously, even after oestrogen pretreatment. The conclusion is drawn that this pressor antagonist may be of value for the prevention of renal cortical necrosis in rats or in human beings.
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PMID:Histochemical and ultrastructural study of renal cortical necrosis in rats treated with oestrone + vasopressin, and its prevention with a vasopressin antagonist. 381

In human fetus, newborn, infant and adult hypothalami, antibodies to ovine corticoliberin-41 stain a paraventriculo-infundibular neuroglandular pathway. The perikarya are located in the paraventricular nucleus, they mainly project to the ventral and lateral areas of the median eminence. Eminential corticoliberin-positive fibres appear during the 16th week of fetal life, and increase in number during the following weeks. Perikarya were first revealed in the 19th week. In some areas of the median eminence, corticoliberin-, vasopressin- or [Met]enkephalin-immunoreactive terminals are similarly distributed. Sequential stainings or staining comparison of contiguous semi-thin sections failed to prove the coexpression of corticoliberin and [Met]enkephalin immunoreactivities in fibres, but indicated that corticoliberin and vasopressin immunoreactivities may be coexpressed in a few fibres. Those methods enabled us to observe, in the paraventricular nucleus, perikarya revealed by corticoliberin and vasopressin antisera. Our results suggest a possible release of corticoliberin in portal vessels of the median eminence beginning in the 16th week of fetal life, i.e. 8 weeks later than appearance of the corticotrophs in the pituitary. Establishment of a corticoliberin hypothalamic control of pituitary corticotrophs at mid gestation agrees with previous physiological and teratological studies. Abundance, as well as immunostaining intensity of the corticoliberin processes, in the infant and adult median eminence attest to the physiological importance of this system. Close vicinity of corticoliberin, vasopressin and [Met]enkephalin fibres, in some eminential areas and coexpression of corticoliberin and vasopressin immunoreactivities in some neurons, are morphological correlates of functional relations which were reported.
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PMID:Anatomical and ontogenetic studies of the human paraventriculo-infundibular corticoliberin system. 387 29

An oxytocin/bovine neurophysin I biosynthetic precursor, [N epsilon-diacetimidyl-30,71, des-His106]pro-OT/BNPI, was synthesized from a synthetic oxytocinyl peptide, 1/2Cys-Tyr-Ile-Gln-Asn-1/2Cys-Pro-Leu-Gly-Gly-Lys-Arg, and native neurophysin by chemical semisynthesis. The semisynthetic precursor contains the entire sequence of the biosynthetic precursor deduced from the complementary DNA structure except for omission of the carboxyl-terminal histidine residue. The covalent structure of the semisynthetic product was verified by amino acid analysis and amino-terminal analysis. Analytical affinity chromatography was employed to evaluate noncovalent binding properties of the precursor. The precursor does not bind significantly to immobilized Met-Tyr-Phe, a hormone binding site ligand. In contrast, the acetimidated precursor binds to immobilized bovine neurophysin II, with a 13-fold higher affinity than does acetimidated neurophysin itself. When a hormonal ligand, [Lys8]vasopressin, was added to the elution buffer at the concentration of 0.1 mM so that a major portion of the immobilized BNPII was liganded, the affinity between the immobilized liganded BNPII and the precursor was enhanced 8-fold and approached the affinity for the liganded (bovine neurophysin I-immobilized BNPII) interaction. The data imply that the precursor can self-associate and that this self-association is closely related to that of liganded neurophysin. The tripeptide affinity matrix data argue that, in the precursor, the ligand binding site of the neurophysin domain is occupied intramolecularly by the hormone domain. The data verify the view that both the self-association surface and hormone binding site are established upon precursor folding. A disulfide stability analysis showed the resistance, to disulfide interchange by dithiothreitol, of semisynthetic precursor but not of neurophysin, as judged by protein association and peptide ligand binding activities, respectively. The results argue that the molecular structure of the precursor is established upon precursor folding and before enzymatic processing that produces mature hormone and neurophysin.
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PMID:Molecular properties of the oxytocin/bovine neurophysin biosynthetic precursor. Studies using a semisynthetic precursor. 400 99

Intraventricular administration of 1,6-aminosuberyl-arginine8-vasopressin or somatostatin in rats barrel rotation, a peculiar rotation along the sagittal body axis. The vasopressin-induced barrel rotation was markedly enhanced by fluphenazine, haloperidol, 6-hydroxydopamine or alpha-methyl-p-tyrosine but was unaffected by (D-Ala2, MePhe4, Met(O)5-ol)-enkephalin. The enhancement of the rotation behavior of fluphenazine was prevented by pretreatment with trihexy-phenidyl a muscarinic receptor blocker. These observations clearly show that vasopressin can elicit barrel rotation and that dopaminergic inhibition and cholinergic activation are concomitantly involved.
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PMID:Barrel rotation induced by vasopressin and involvement of dopaminergic and cholinergic functions in rats. 611 18

Immunoreactive-vasopressin, -oxytocin, -dynorphin, -dynorphin-(1-8), -alpha-neo-endorphin and -[Met]enkephalin were, in each case, present in greater concentrations in dorsal as compared to ventral, and lumbo-sacral as compared to cervico-thoracic, spinal cord. These differences were significantly more pronounced for vasopressin and oxytocin than for the other peptides. Lesions of the hypothalamic paraventricular nucleus depleted levels of immunoreactive-vasopressin and -oxytocin throughout the cord whereas levels of the opioid peptides therein were unaffected. In contrast, destruction of either the supraoptic or suprachiasmatic nucleus failed to change the content of immunoreactive-vasopressin, -oxytocin or any of the opioid peptides in the cord. Dehydration for 3 days depressed levels of immunoreactive-vasopressin, -oxytocin and -dynorphin in the neurointermediate lobe of the pituitary. In distinction, the levels of these were not modified in the spinal cord. Further, treatment with the synthetic corticosteroid, dexamethasone, elevated levels of immunoreactive-vasopressin, -oxytocin and -dynorphin in the neurointermediate pituitary whereas these were unaffected in the spinal cord. It is concluded that vasopressin and oxytocin in the spinal cord are predominantly derived from the paraventricular nucleus, localized in dorsal lumbo-sacral regions of the cord and insensitive to endocrinological manipulations. These pools may, thus, be modulated differently from their counterparts in the neurohypophysis and have a differing role, possibly in the control of the primary processing, autonomic or motor junctions. Further, there is no evidence from these or our prior studies for a close interrelationship of spinal cord vasopressin with dynorphin-related peptides (or oxytocin with [Met]enkephalin), likewise in contrast to the neurohypophysis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Vasopressin and oxytocin in the rat spinal cord: distribution and origins in comparison to [Met]enkephalin, dynorphin and related opioids and their irresponsiveness to stimuli modulating neurohypophyseal secretion. 614 93


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