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)

Specific binding sites for somatostatin have been characterized in cytosolic fraction of rabbit renal papilla. The interaction of 125I-Tyr11-somatostatin with cytosolic fraction was rapid, reversible, specific, saturable and dependent on temperature. At 25 degrees C the binding data were compatible with the existence of two classes of binding sites: a high-affinity class with a Kd = 57.7 nM and a low-affinity class with a Kd = 217.4 nM. Somatostatin binding sites exhibited a high degree of specificity since neuropeptides such as Leu-enkephalin, neurotensin, substance P, vasopressin and vasoactive intestinal peptide behaved as ligands with null or very low affinity.
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PMID:Interaction of somatostatin with isolated cytosol from rabbit renal papilla. 287 74

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

Steroid hormones modify several brain functions, at least in part by altering expression of particular genes. Of interest are those genes that are involved in cell-cell communication in the brain, for instance neuropeptide genes and genes that code for enzymes involved in synthesis of neurotransmitters. Steroid regulation of mRNA levels for several genes has been reported, including the genes coding for the neuropeptides vasopressin, corticotropin releasing factor, luteinizing hormone-releasing factor, pro-opiomelanocortin; somatostatin, preproenkephalin, and the enzyme tyrosine hydroxylase. Steroid control of releasing factor genes is consistent with classical neuroendocrine concepts of negative feedback. Steroid-induced plasticity of gene expression is sometimes in evidence, with the presence or absence of a particular steroid inducing expression of a neuropeptide gene in neurons that under other conditions do not express the gene. As a means of gaining some insight into the mechanism of action of steroid hormones, several groups have determined some of the neuropeptide profiles of neurons that contain receptors for steroid hormones. Marked heterogeneity is found, in that often only a subpopulation of phenotypically-similar neurons, even within a single brain area, contains receptors for a given steroid.
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PMID:Regulation of neuropeptide gene expression by steroid hormones. 307 66

Rat neurointermediate lobes and neurohypophyses separated from the pars intermedia were stimulated in vitro in the presence of either D-Ala2, D-Leu5-enkephalin (DADLE), a Leu-enkephalin stable analogue or FK 33-824 a Met-enkephalin stable analogue. Secretion of vasopressin (AVP) and oxytocin (OT) was produced by either a Ca2+-ionophore or with electrical stimulation or by K+-induced depolarization. These opioid peptides and their antagonist naloxone did not affect basal nor evoked hormone release. Furthermore, they did not affect the evoked calcium uptake induced with electrical stimulation. These findings were confirmed using a preparation of isolated neurosecretory nerve endings. Further, dopamine had no effect on the K+-induced AVP release although a crude extract of the pars intermedia abolished the electrically-evoked and reduced considerably the potassium-evoked AVP release. It is concluded that in the neurohypophysis neither Leu- and Met-enkephalin nor dopamine affect the secretion-coupling mechanism at the level of the neurosecretory nerve endings.
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PMID:Do opioid peptides modulate, at the level of the nerve endings, the release of neurohypophysial hormones? 351 53

Isolated rat pituitary stalk-neurohypophysial complexes were electrically stimulated and the evoked compound action potentials were recorded at the level of both axons and nerve terminals. The latency of the nerve terminal response increased during continuous stimulation of the stalk at frequencies as low as 1 Hz. At similar frequencies continuous stimulation of the stalk produced an increase in the latency of the response of the nerve fibres and a decrease in the amplitude of the compound action potential. The increase in the latency of the response of both axons and nerve terminals was related to the frequency and number of stimuli. The time necessary for full recovery of the response of the axons and the nerve endings, following stimulation at frequencies above 5 Hz, was not linearly related to the frequency of stimulation. Stimulation of the stalk with a pulse pattern (bursts) imitating the electrical activity of vasopressin-containing magnocellular neurones showed that the latency of the compound action potential had increased by the end of the first burst. The latency of the response of axons and nerve endings was inversely proportional to the time interval between bursts. Prolonged stimulation of the isolated neural lobe with 'vasopressin'-like bursts induced the release of vasopressin. Twelve bursts, separated by 3 min intervals, released more hormone than fifty bursts given during the same period of time, but separated by a 21 s interval. Leu-enkephalin (10(-5) M) did not modify the latency or the amplitude of the action potentials evoked with low frequency of stimulation (0.5 Hz) or with 'vasopressin'-like bursts. In conclusion, it is suggested that the electrical properties of the nerve fibres and the nerve endings goes some way to explain the pattern of hormone release observed during sustained stimulation.
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PMID:Electrical properties of axons and neurohypophysial nerve terminals and their relationship to secretion in the rat. 361 74

We report our experience in development of the in situ hybridization (ISH) procedure to detect messenger RNAs (mRNAs) coding for various molecules involved in endocrine glands and central nervous system activity, including mRNAs coding for endorphin precursors [preproenkephalin A (PPA), pro-opiocortin (POMC)], vasopressin, and transferrin. Various conditions of fixation and handling of the tissues were tested to establish optimal parameters for mRNA detection. Double-stranded DNA probes labeled by nick translation, synthetic oligonucleotides labeled at their 5' end, as well as single-stranded RNA probes were used, after incorporation of 32P- or 35S-labeled nucleotides. Specific requirements for efficient and reproducible ISH investigations are discussed. Cells expressing the PPA gene in the adrenal medulla and in the brain were detected by ISH. The results show that ISH is as sensitive as immunohistochemistry in detecting peptide-producing cells in the adrenal and that it allows detection of PPA cell bodies in brain in conditions in which they are inconstantly detected by immunohistochemistry. Unilateral destruction of substantia nigra provokes a dramatic decrease in the number of neurons expressing the PPA gene in the contralateral striatum. Cells expressing the POMC gene were detected in the pituitary of various species including man and in the rat arcuate nucleus. Neurons containing vasopressin mRNA were visualized in the supraoptic paraventricular and suprachiasmatic nucleus of the adult rat by using a synthetic oligonucleotide probe. Transferrin gene expression was shown in the central nervous system of the rat brain in two cell populations, the oligodendrocytes and the epithelial cells of the choroid plexus, by demonstration of simultaneous presence in them of transferrin immunoreactivity together with transferrin mRNA. These results show that the ISH procedure is a technique that can be routinely used to investigate gene transcription anatomically in complex heterocellular tissues such as the endocrine glands and the nervous system.
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PMID:In situ hybridization histochemistry for the analysis of gene expression in the endocrine and central nervous system tissues: a 3-year experience. 375 62

This study examines the effect of leu-enkephalin on K+, veratridine and isoproterenol stimulation of vasopressin (AVP) release from perifused neurointermediate pituitaries of rats. As opposed to catecholamine-evoked release of peptide, the secretory response to high K+ and veratridine involves Ca2+ influx, as the effect of both factors was blocked by Ca-chelation and the channel blocker D 600. Leu-enkephalin was found to antagonize AVP secretion induced by K+ and veratridine depolarization, by acting through a naloxone-sensitive receptor system. In contrast, the opiate failed to significantly affect isoproterenol-stimulated release of AVP, which we show to be correlated to cAMP accumulation in pure neurohypophyseal tissue. These results support the view that opiates modulate AVP secretion triggered by depolarization of nerve terminals by regulating Ca2+ fluxes.
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PMID:Modulation by leu-enkephalin of peptide release from perifused neurointermediate pituitary. I. Selective effect on potassium-, veratridine- and isoproterenol-stimulated secretion of vasopressin. 609 48

The distribution of immunoreactive leu-enkephalin neurons and fibers in the monkey hypothalamus, including ultrastructural localization in the paraventricular nucleus (PVN), was examined with the peroxidase-antiperoxidase immunocytochemical method. Immunoreactive leu-enkephalin cell bodies and fibers were present in the PVN, the region of the dorsal nucleus and nucleus of the anterior commissure, the dorsomedial nucleus, ventromedial nucleus, and lateral hypothalamus. Within the PVN labeled cells were found mostly in the medial parvocellular region, and a smaller proportion including some large cells was present in the lateral, and dorsolateral zones. Immunoreactive neurons contained numerous large granular vesicles (LGV) which ranged from 63 to 235 nm in size, suggesting that at least some enkephalin-containing neurons belong to the population of neurosecretory cells. Positive neurons were postsynaptic to four types of unlabeled axon terminals. Leu-enkephalin-containing fibers (some of which were myelinated) and boutons contained small clear vesicles and numerous LGV. Axon terminals made synaptic contacts with the cell bodies, primary and distal dendrites of unlabeled neurons. The findings show that enkephalin-containing neurons in the PVN integrate a variety of neuronal inputs and provide morphological evidence for the inhibiting influence of enkephalins on the firing rate of PVN neurons. It may be speculated that the effects of opioids on the release of vasopressin and other substances possibly originating from PVN neurons may be regulated in part within the nucleus by locally synapsing axons belonging to enkephalin-containing neurons.
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PMID:Immunoreactive leu-enkephalin in the monkey hypothalamus including observations on its ultrastructural localization in the paraventricular nucleus. 614 2

Immunohistochemical studies of the vas deferens and seminal vesicle of mouse, guinea-pig, and rabbit showed the presence of nerve fibres containing vasoactive intestinal polypeptide (VIP), substance P (SP), and gastrin-releasing peptide (GRP) supplying the smooth muscle layers as well as blood vessels. The nerve supply was better developed in the seminal vesicle than in the vas deferens. The motor activity of the vas deferens and seminal vesicle of the guinea-pig was studied in vitro. The vas deferens responded to transmural electrical stimulation with a twitch followed by a slow contraction. The twitch was blocked by guanethidine and tetrodotoxin, but not by atropine, propranolol, phenoxybenzamine, or fluphenazine. The slow contraction exhibited features of an alpha-receptor-mediated response. SP, physalaemin and eledoisin contracted the smooth muscle and also potentiated the twitch response to electrical nerve stimulation in a concentration-dependent manner. The SP blocking agent, (D-Pro2,D-Trp7,9)-SP, affected neither the resting tension nor the response to electrical stimulation. It is therefore suggested that the SP fibres act mainly prejunctionally. VIP, Leu-enkephalin, cholecystokinin octapeptide (CCK-8), angiotensin II, vasopressin, neurotensin, bombesin, and GRP had no effect on either the resting tension or the response to electrical nerve stimulation. The seminal vesicle responded to electrical stimulation with a contraction which was unimpaired by atropine, propranolol, phenoxybenzamine, and guanethidine, but abolished by tetrodotoxin. Hence, this contraction is mediated by a non-adrenergic, non-cholinergic neurotransmitter. Bombesin, GRP, SP, physalaemin and eledoisin contracted the smooth muscle and potentiated the response to electrical stimulation. VIP, Leu-enkephalin, CCK-8, angiotensin II, vasopressin, and neurotensin had no effect on the resting tension or on the response to transmural electrical stimulation. The SP antagonist abolished the contraction elicited by SP but did not influence the response to nerve stimulation. The results suggest that the SP and GRP nerves may have prejunctional and facilitating postjunctional effects in the seminal vesicle.
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PMID:Immunohistochemical localization of substance P, vasoactive intestinal polypeptide and gastrin-releasing peptide in vas deferens and seminal vesicle, and the effect of these and eight other neuropeptides on resting tension and neurally evoked contractile activity. 619 10

Opioid peptides were localized in fibres of the rat neural lobe using various immunocytochemical methods at the light- and electron-microscopical level. Leu-enkephalin immunoreactivity was present in beaded fibres distributed throughout the neural lobe. These fibres surround the neurohypophyseal glial cells (pituicytes) and make synaptoid contacts upon their soma and processes. The reaction product was localized both in dense-core vesicles of about 100 nm in diameter and diffusely spread over the cytoplasm. No arguments in support of the co-existence of enkephalins and the neurohypophyseal hormones vasopressin and oxytocin in the same terminal were found. It is suggested that pituicytes might mediate the inhibitory effect of opiod peptides on vasopressin and oxytocin release from the neural lobe.
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PMID:Enkephalin immunoreactivity in synaptoid elements on glial cells in the rat neural lobe. 634 78


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