UNIPROT:P01185 - FACTA Search

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Query: UNIPROT:P01185 (vasopressin)
23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a previous study (Watts et al., '87) we reexamined the projections of the suprachiasmatic nucleus (SCh) with the PHA-L method and found that they could be divided conveniently into six groups of fibers. By far the densest projection ends just dorsal to the SCh in a comma-shaped region designated the "subparaventricular zone," although some fibers continue on through the paraventricular nucleus of the hypothalamus to end in the overlying midline thalamus, and others continue on to end in the dorsomedial nucleus, the region around the ventromedial nucleus, and the posterior hypothalamic area. Other relatively sparse projections from the SCh were also described to the preoptic region, lateral septal nucleus, parataenial and paraventricular nuclei of the thalamus, and ventral lateral geniculate nucleus. In addition, the same method was used to show that the subparaventricular zone projects in turn massively to these same regions, as well as back to the SCh itself and to the periaqueductal gray. The present series of experiments was designed to confirm these observations with retrograde tracer injections and to investigate the cellular and possible neurotransmitter organization of the major projections from the SCh and subparaventricular zone with a combined retrograde tracer-immunohistochemical method. For this, the distribution of neuronal cell bodies within the SCh that stain with antisera to vasopressin, vasoactive intestinal polypeptide (VIP), corticotropin-releasing factor, bombesin, substance P, neurotensin, somatostatin, thyrotropin-releasing hormone, and angiotensin II was described in detail first. Then the distribution of retrogradely labeled neurons that were also stained for one or another of these peptides was described after injections of true blue, or in some cases SITS, into the regions of the subparaventricular zone, the paraventricular and parataenial nuclei of the thalamus, the ventromedial nucleus, the dorsomedial nucleus, and the periaqueductal gray. The results confirm previous immunohistochemical and anterograde tracing studies and in addition indicate that cells in dorsal as well as ventral parts of the SCh project to each of the terminal fields examined, as do many cells in surrounding areas, including the subparaventricular zone. Our results also suggest that, at the very least, vasopressin-, VIP-, and neurotensin-stained cells in the SCh project to the subparaventricular zone, midline thalamus, and dorsomedial nucleus, and that the vasopressin and VIP-stained fiber systems are partially segregated at the level of the subparaventricular zone.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Efferent projections of the suprachiasmatic nucleus: II. Studies using retrograde transport of fluorescent dyes and simultaneous peptide immunohistochemistry in the rat. 243 9

In the search for a more potent bombesin antagonist, we found [D-Arg1,D-Phe5,D-Trp7,9,Leu11]substance P to be effective in mouse fibroblasts and to inhibit the growth of small cell lung cancer, a tumor that secretes bombesin-like peptides that may act as autocrine growth factors. In murine Swiss 3T3 cells, [D-Arg1,D-Phe5,D-Trp7,9,Leu11]substance P proved to be a bombesin antagonist as judged by the following criteria: (i) inhibition of DNA synthesis induced by gastrin-releasing peptide and other bombesin-like peptides; (ii) inhibition of 125I-labeled gastrin-releasing peptide binding to the bombesin/gastrin-releasing peptide receptor; (iii) reduction in cross-linking of the Mr 75,000-85,000 protein putatively a component of the bombesin/gastrin-releasing peptide receptor; (iv) blocking of early cellular events that precede mitogenesis--calcium mobilization and inhibition of epidermal growth factor binding. [D-Arg1,D-Phe5,D-Trp7,9,Leu11]substance P was 5-fold more potent than the antagonist [D-Arg1,D-Pro2,D-Trp7,9,Leu11]substance P. [D-Arg1,D-Phe5,D-Trp7,9,Leu11]substance P also inhibits mitogenesis induced by vasopressin but not that induced by a variety of other mitogens. Both antagonists reversibly inhibited the growth of small cell lung cancer in vitro in a concentration-dependent manner. Peptide antagonists could, therefore, have far-reaching therapeutic implications.
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PMID:[D-Arg1,D-Phe5,D-Trp7,9,Leu11]substance P, a potent bombesin antagonist in murine Swiss 3T3 cells, inhibits the growth of human small cell lung cancer cells in vitro. 245 Mar 49

A nonselective cation channel that we characterized in the mouse L-cell membrane becomes quiescent with serum deprivation (arrested cell growth) and rapidly active upon readdition of serum or, specifically, platelet-derived growth factor (PDGF). Using the patch-clamp technique, we find that the predominant channel in the LMTK- cell line is a bursting nonselective cation channel (the NS channel). In cell-attached and inside-out patches, the channel has a conductance of 28 pS; equal selectivity for Na+, K+, and Cs+; and no anion or divalent cation permeability. The channel open probability is voltage insensitive and in inside-out patches does not correlate with intracellular calcium (0.5 nM to 50 microM). When cultures are rendered quiescent by incubation in serum-free medium, channel open probability is virtually 0 as compared to 0.26 (+/- 0.17) in exponentially growing cultures. If mitogenesis is initiated by readdition of serum to quiescent cells while maintaining cell-attached recording, there is a rapid (15-30 s) activation of the channel (n = 12). The open probability of the patch increases (greater than 0.75) for 2-3 min and then decreases. We have attempted applications of several growth factors (fibroblast-derived growth factor, epidermal growth factor, insulin, bombesin, alpha-thrombin, and vasopressin, individually or in combination) but find that only PDGF (5-100 ng/ml; n = 9) produces channel activation. This activation should provide a Na+ entry pathway parallel to that of the Na/H exchanger.
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PMID:Activation of single-channel currents in mouse fibroblasts by platelet-derived growth factor. 246 5

We have examined the distribution pattern and the density of various neuropeptide, neurotransmitter and enzyme containing neurons in the rat medial septum and the nucleus of the diagonal band of Broca to assess their possible involvement in the septohippocampal, septocortical and septobulbar pathways. Immunohistochemical methods were combined with the retrograde transport of a protein-gold complex injected in the hippocampus, the cingulate cortex or the olfactory bulb. Cholinergic neurons were the most numerous. Galanin-positive neurons were about two or three times less numerous than cholinergic cells. Both these cell types had a similar location though the choline acetyl transferase-like immunoreactive cells extended more caudally in the horizontal limb of the nucleus of the diagonal band of Broca. Immunoreactive cells for other neuroactive substances were few (calcitonin gene-related peptide, luteinizing hormone releasing hormone. [Met]enkephalin-arg-gly-leu) or occasional (dynorphin B, vasoactive intestinal polypeptide, somatostatin, neurotensin, cholecystokinin, neuropeptide Y and substance P). No immunoreactive cells for bombesin, alpha atrial natriuretic factor, corticotropin releasing factor, 5-hydroxytryptamine, melanocyte stimulating hormone, oxytocin, prolactin, tyrosine hydroxylase or arg-vasopressin were present. Choline acetyltransferase- and galanin-like immunoreactive cells densely participate to septal efferents. Cholinergic neurons constituted the bulk of septal efferent neurons. Galanin-positive cells were 22% of septohippocampal, 8% of septocortical, and 9% of septobulbar neurons. Galanin containing septohippocampal neurons were found in the medial septum and the nucleus of the diagonal band of Broca; galanin-positive septobulbar and septocortical cells were limited to the nucleus of the diagonal band of Broca. Occasional double-labellings were noticed with some peptides other than galanin. Luteinizing hormone-releasing hormone, calcitonin gene-related peptide and enkephalin were the most often observed; some other projecting cells stained for vasoactive intestinal polypeptide or dynorphin B. Luteinizing hormone-releasing hormone, calcitonin gene-related peptide and enkephalin were observed in septohippocampal neurons; luteinizing hormone-releasing hormone and vasoactive intestinal peptide were observed in septocortical neurons and calcitonin gene-related peptide, luteinizing hormone-releasing hormone and dynorphin B were observed in septo-bulbar cells. These results show that, in addition to acetylcholine, galanin is a major cellular neuroactive substance in septal projections to the hippocampus, the cingulate cortex and the olfactory bulb. The presence of septal projecting neurons immunoreactive for other peptides shows that a variety of distinct peptides may also participate, but in a smaller number, to septal efferent pathways.
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PMID:Cholinergic and peptidergic projections from the medial septum and the nucleus of the diagonal band of Broca to dorsal hippocampus, cingulate cortex and olfactory bulb: a combined wheatgerm agglutinin-apohorseradish peroxidase-gold immunohistochemical study. 247 18

Changes in intracellular free Ca2+ concentration [( Ca2+]i) produced by growth factors and mitogens have been studied using aequorin-loaded Swiss 3T3 cells. Decreasing free Ca2+ in the external medium by using EGTA had no significant effect on the increase in [Ca2+]i produced by vasopressin, bradykinin, bombesin or prostaglandin E2, but reduced the increase in [Ca2+]i produced by platelet derived growth factor (PDGF) by 58%, by prostaglandin E1 44% and by prostaglandin F2 alpha 47%. The dihydropyridine Ca2+-channel antagonist nifedipine at 10 microM inhibited the [Ca2+]i response to PDGF by 41% in both the presence of and in the absence of external Ca2+. Methyl-1,4-dihydro-2,6-dimethyl-3-nitro-4-(2-trifluoromethylphenyl) pyridine-5-carboxylate (BAY K8644), a Ca2+-channel agonist, at 10 microM produced an increase in [Ca2+]i and decreased the [Ca2+]i response to PDGF by 39%. Nifedipine did not block 45Ca2+ uptake or release by inositol 1,4,5-trisphosphate in saponin-permeabilized Swiss 3T3 fibroblasts but BAY K8644 inhibited 45Ca2+ release by inositol 1,4,5-trisphosphate. The results suggest that the increase in [Ca2+]i caused by PDGF in Swiss 3T3 fibroblasts is due to the influx of external Ca2+ through dihydropyridine sensitive Ca2+ channels, as well as release of internal Ca2+.
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PMID:Contribution of external and internal Ca2+ to changes in intracellular free Ca2+ produced by mitogens in Swiss 3T3 fibroblasts: the role of dihydropyridine sensitive Ca2+ channels. 247 47

The purpose of the present study was to quantify the extent to which several peptides and serotonin coexist with substance P or somatostatin in selected lumbar dorsal root ganglia of the cat. The technique for the simultaneous visualization of two antigens by immunofluorescence was used to investigate the coexistence of neuropeptides in the lumbar dorsal root ganglia of colchicine-treated cats. Perikarya immunoreactive for calcitonin gene-related peptide, galanin, leu-enkephalin, somatostatin, and substance P were visualized in both the lumbar 5 and 6 dorsal root ganglia. In contrast, no immunoreactivity was observed for adipokinetic hormone, bombesin, dynorphin A, met-enkephalin, oxytocin, tyrosine hydroxylase, thyrotropin-releasing hormone, vasopressin, vasoactive intestinal peptide, or serotonin in either ganglion examined. Substance P coexisted with calcitonin-gene-related peptide, somatostatin, and leu-enkephalin. Somatostatin was colocalized with calcitonin gene-related peptide, leu-enkephalin, and substance P but coexisted with galanin minimally. The cell area of immunoreactive perikarya was also examined. Data concerning the cross-sectional area of immunoreactive cells indicated that somatostatin-immunoreactive perikarya were generally the largest population observed (up to approximately 6,000 microns2). Somatostatin and calcitonin gene-related peptide, as well as substance P and calcitonin gene-related peptide, coexisted in populations of cell bodies that had a smaller size (less than 2,000 microns2). These results suggest that certain peptides which coexist in the dorsal root ganglia may provide histochemical markers for functional groups of primary afferent neurons.
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PMID:Lumbar dorsal root ganglia of the cat: a quantitative study of peptide immunoreactivity and cell size. 247 1

While screening neuropeptides for activity as growth factors we have found that bradykinin is a mitogen for Swiss 3T3 cells. It acts synergistically with insulin, and maximal effect is obtained at 10 nM. It acts through a distinct receptor, characterized as a B2 subtype using bradykinin analogues. The neuropeptides bombesin and vasopressin are also potent mitogens for Swiss 3T3 cells. The substance P antagonists [DArg1, DPro2, DTrp7,9, Leu11] substance P and [DArg1, DPhe5, DTrp7,9, Leu11]substance P are inhibitors of DNA synthesis stimulated by both bombesin and vasopressin. In the present study they were found also to inhibit bradykinin-induced mitogenesis. In contrast, the ligand-specific antagonists [Leu13-psi(CH2NH)Leu14]bombesin, [Pmp1, OMeTyr2, Arg8]vasopressin and [DArg0, Hyp3, Thi5,8, DPhe7]bradykinin showed no cross-inhibition with each others receptors. We propose therefore that the receptors for the mitogenic neuropeptides bombesin, vasopressin, and bradykinin can interact with two classes of antagonist, one recognizing the ligand binding site (e.g., [Leu13-psi(CH2NH)Leu14]bombesin) and the other recognizing a common domain shared by the three receptors (e.g., [DArg1, DPhe5, DTrp7,9, Leu11]substance P).
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PMID:Two classes of antagonist interact with receptors for the mitogenic neuropeptides bombesin, bradykinin, and vasopressin. 248 37

Single-cell fluorescence image analysis has been used to characterize the mitogen-induced increases in intracellular free [Ca2+] ([Ca2+]i) in control and protein kinase C-depleted Swiss 3T3 cells. More than 80% of the control cells exhibited fast, transient responses to bombesin, vasopressin, or prostaglandin F2 alpha (PGF2 alpha). In contrast, the [Ca2+]i responses induced by platelet-derived growth factor (PDGF) were markedly more heterogeneous, slower, and often biphasic, with fewer cells (60-70%) responding. The peak [Ca2+]i values obtained in response to each mitogen showed substantial variation between cells. Brief pretreatment of the cells with 12-O-tetradecanoyl phorbol 13-acetate (TPA) reduced the [Ca2+]i responses to bombesin, but did not affect the responses to PDGF. Long-term pretreatment of the cells with TPA to down-modulate protein kinase C resulted in substantially prolonged [Ca2+]i responses to bombesin, vasopressin, and PGF2 alpha, but had no such effect on the responses to PDGF. We conclude that differences between the [Ca2+]i responses to bombesin and PDGF, previously reported using cell populations, reflect differences occurring in individual cells, and that the [Ca2+]i responses to bombesin, vasopressin, and PGF2 alpha (but not PDGF) are subject to feedback inhibition via protein kinase C.
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PMID:Single-cell analysis of the mitogen-induced calcium responses of normal and protein kinase C-depleted Swiss 3T3 cells. 251 20

Insulin and various growth factors (epidermal growth factor (EGF), insulin-like growth factor, fibroblast growth factor, and transforming growth factor alpha), which fail to modify the resting [Ca2+]i in PC12 rat pheochromocytoma and SKNBE human neuroblastoma cells when administered alone, became capable of inducing [Ca2+]i increases when administered a few (4-20) min after another agent, bradykinin. The latter peptide, working through a B2 receptor, caused hydrolysis of polyphosphoinositides and a large, biphasic [Ca2+]i transient (an initial (1-2 min) spike, originated primarily from intracellular stores, followed by a steady-state elevation dependent on Ca2+ influx). Priming by bradykinin of the growth factor effects was quickly dissipated by the addition of a B2 blocker. Activation of other receptors coupled to polyphosphoinositide hydrolysis: muscarinic and purinergic (in PC12 and SKNBE cells); bombesin and vasopressin receptors (in Swiss 3T3 cells), was without effect in priming. Bradykinin-primed, growth factor-induced [Ca2+]i rises in PC12 cells appeared after a 20-30-s delay; they were relatively small, but persistent; their concentration dependence was similar to that of other effects of the factors; and they included both release of Ca2+ from intracellular stores and stimulation of Ca2+ influx, preceded (in PC12 cells) by a transient increase of polyphosphoinositide hydrolysis. Thus the effect of growth factors (possibly dependent on the tyrosine kinase activity of their receptors) consisted in the reinforcement of the transmembrane signaling at B2 receptors. This is the first direct demonstration of a [Ca2+]i rise induced by insulin and insulin-like growth factor-I, and of such an effect of EGF in cell types endowed with a small number of specific EGF receptors.
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PMID:Reinforcement of signal generation at B2 bradykinin receptors by insulin, epidermal growth factors, and other growth factors. 253 35

Prolonged exposure of quiescent Swiss 3T3 cells to vasopressin prevents mitogenic stimulation on subsequent addition of bombesin. This heterologous desensitization is selective and can be mimicked by vasopressin agonists, including [Lys8]vasopressin and oxytocin but not by the V1-type-specific vasopressin receptor antagonist [Pmp1,O-Me-Tyr2,Arg8]vasopressin [where Pmp is 1-(beta-mercapto-beta,beta-cyclopenthamethylene propionic acid)]. Furthermore, vasopressin-induced loss of responsiveness to bombesin can be blocked by addition of this antagonist, indicating that heterologous desensitization is mediated through the vasopressin receptor. Desensitization requires prolonged incubation (half-maximal desensitization occurring after approximately 20 hr of pretreatment) and continuous protein synthesis. Bombesin responsiveness is restored by incubation in the absence of vasopressin. Pretreatment does not alter the number, affinity, or internalization capacity of the bombesin receptors. However, the induction of the protooncogene c-fos by bombesin is profoundly inhibited after vasopressin pretreatment. We suggest that the coupling of the activated bombesin receptor to the generation of its early signals is impaired in desensitized cells.
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PMID:Heterologous desensitization of bombesin-induced mitogenesis by prolonged exposure to vasopressin: a post-receptor signal transduction block. 254 35

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