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)

Neuropeptide Y (NPY), acting through various medial hypothalamic nuclei, is found to have potent effects on a variety of endocrine, physiological and behavioral systems that modulate energy balance. This peptide affects the release of various hormones, such as corticosterone, insulin, aldosterone and vasopressin, which modulate energy metabolism, as well as food intake. It also has direct impact on energy metabolism through an effect on substrate utilization and lipogenesis. Finally, NPY has a remarkably potent stimulatory effect on feeding behavior, which is characterized by a selective increase in carbohydrate ingestion that is strongest at the beginning of the active feeding cycle and is dependent upon circulating levels of corticosterone. This evidence has led to the proposal that NPY exerts anabolic effects to restore energy balance at specific times of energy depletion. Increased NPY activity may occur at the beginning of the active cycle or after a period of food deprivation. Further evidence, that chronic NPY stimulation produces profound hyperphagia and obesity and that endogenous NPY concentration is increased in genetically obese animals, strongly suggests that hypothalamic NPY may contribute to the development of eating disorders and obesity.
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PMID:Brain neuropeptide Y: an integrator of endocrine, metabolic and behavioral processes. 195 27

The effects of transient (30') forebrain ischemia (4 vessel occlusion model) on peptidergic neurons and astroglial cells in various diencephalic and telencephalic areas have been analyzed. The study was performed at various time intervals of reperfusion, i.e. 4 h, 1, 7 and 40 days. Neuropeptide Y (NPY), somatostatin (SRIF), cholecystokinin (CCK), vasoactive intestinal polypeptide (VIP) and arginine-vasopressin (AVP) immunoreactive (IR) neuronal systems and glial fibrillary acidic protein (GFAP)-IR glial cells have been visualized by means of the indirect immunoperoxidase procedure using the avidin-biotin technique. The analysis was performed by means of computer assisted microdensitometry and manual cell counting. At the hippocampal level a huge reduction of neuropeptide (CCK, SRIF, VIP) IR cell bodies was observed, still present 40 days after reperfusion. On the contrary, in the frontoparietal cortex the number of the neuropeptide (CCK, SRIF, VIP, NPY) IR neurons showed a decrease at 4 h, 1 and 7 days after reperfusion followed by a complete recovery at 40 days. A rapid reduction followed by an almost complete recovery (7 days after reperfusion) was also observed at striatal level where SRIF- and NPY-IR neurons were detected. A marked decrease of NPY-IR terminals was observed in the paraventricular and periventricular hypothalamic nuclei and in the paraventricular thalamic nucleus. AVP-IR was markedly reduced in the magnocellular part of the paraventricular nucleus throughout the analyzed period (7 days after reperfusion). GFAP-IR was increased in the hippocampal formation and neostriatum while a not consistent increase was observed at neocortical level. These data point to a differential recovery of peptide-IR and to a different astroglial response in the various brain areas after transient forebrain ischemia. Region-specific factors rather than factors related to neuronal chemical coding seems to play a major role in determining the vulnerability of neuronal populations to transient ischemia.
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PMID:Effects of transient forebrain ischemia on peptidergic neurons and astroglial cells: evidence for recovery of peptide immunoreactivities in neocortex and striatum but not hippocampal formation. 197 43

Phe-Leu-Phe-Gln-Pro-Gln-Arg-Phe-NH2 (F-8-F-NH2), isolated from bovine brain, is an FMRF-NH2-like peptide with morphine-modulating activity. In the rat, F-8-F-NH2 immunoreactivity (IR) is highly localized in the neurohypophysis. In this study, F-8-F-NH2-IR was studied in the hypothalamo-neurohypophyseal system of an Arg8-vasopressin (AVP)-deficient animal, the Brattleboro (DI) rat, and the normal control Long-Evans (LE) strain. F-8-F-NH2-IR in the DI pituitary is below the level of detection in contrast to that in the LE (0.50 +/- 0.04 pmol/gland). Neuropeptide Y (NPY) levels are increased two-fold in the DI pituitary while AVP levels are below detection. The content of F-8-F-NH2-IR in the hypothalami and spinal cords of DI and LE rats is not statistically different, suggesting that the absence of F-8-F-NH2-IR in the Brattleboro pituitary is not due to a genetic defect in F-8-F-NH2 biosynthesis. The results of this study raise the question whether AVP could be involved in the regulation of F-8-F-NH2 immunoreactivity in the neurohypophysis.
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PMID:FMRF-NH2-like peptide is deficient in the pituitary gland of the Brattleboro rat. 235 58

In the rat hypothalamus, neuropeptide Y-containing neurons first appeared on day 14.5 of gestation in the arcuate nucleus and in the dorsolateral hypothalamic area. Until birth neuropeptide Y-containing cell bodies increased in number in the arcuate, dorsomedial-lateral and paraventricular nuclei, but disappeared thereafter, but some cells remaining in the arcuate nucleus. In animals treated neonatally with monosodium L-glutamate to destroy the arcuate nucleus, neuropeptide Y-immunoreactivity became evident in many cells scattered in the magnocellular paraventricular and dorsomedial-lateral hypothalamic nuclei on day 16 but not on days 60 and 12. These neuropeptide Y-immunoreactive neurons which appeared in the paraventricular nucleus were also vasopressin-positive. Neuropeptide Y fibers, on the contrary, remarkably diminished in number on day 16, particularly in the paraventricular and dorsomedial-lateral nuclei, and the medial preoptic area, but made a considerable recovery on days 60 and 120. Hence it is probable that, in normal ontogenetic progress, the development of the neuropeptide Y fibers in these areas is inhibitorily affected by that of arcuate neuropeptide Y neurons.
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PMID:Development of the neuronal system containing neuropeptide Y in the rat hypothalamus. 277 71

a) In the hypothalamus, NPY immunoreactive neurons are non catecholamine containing neurons whereas in the medulla oblongata NPY is present in the majority of the catecholamine neurons. NPY immunoreactive neurons in the MO are critically located at the site of the baroreceptor afferents termination. b) High densities of receptors, as indicated by 125I-pNPY binding studies are present in the various subnuclei of the NTS and area postrema. In slice preparations of this region NPY reduces forskolin and phorbolester-induced cAMP accumulation. c) Antagonistic interactions between NPY-and alpha 2-receptors exist in the NTS. d) Neuropeptide Y and adrenaline both lower the mean arterial blood pressure, heart and respiratory rates after central administration. When given together they antagonize the hypotensive but not the respiratory response of each other. e) Central NPY administration leads to alterations in serum levels of corticosterone, aldosterone, angiotensin II, vasopressin, PRL, LH, GH and TSH which are parallel to changes in discrete hypothalamic catecholamine neuronal systems. f) It is proposed that NPY is a transmitter involved in central cardiovascular and neuroendocrine regulation operating in close association with the CA systems. Before the precise role of NPY can be established, however, specific antagonists have to be developed.
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PMID:Brain neuropeptide Y mechanisms. Basic aspects and involvement in cardiovascular and neuroendocrine regulation. 282 7

Neuropeptide Y (NPY) is known to potentiate the pressor effect of norepinephrine. In the present work, we evaluated in unanesthetized normotensive rats the effect of NPY on blood pressure responsiveness not only to norepinephrine, but also to tyramine, a sympathomimetic agent acting indirectly to B-HT933, a selective alpha-2 adrenoceptor stimulant, to angiotensin II and vasopressin. Dose-response curves to the various pressor agents were established starting at the 45th min of an i.v. infusion with either NPY (0.025 and 0.1 microgram/min) or its vehicle. The two doses of NPY increased blood pressure by an average of approximately 6 mm Hg, which was not significantly different from the vehicle-induced blood pressure changes. NPY significantly enhanced the pressor effect of norepinephrine, tyramine and angiotensin II, but not that of B-HT933 and vasopressin. We also tested whether NPY inhibits the enzyme activity of Na, K-adenosine triphosphatase using a purified toad kidney preparation. Concentrations of NPY from 10(-14) M up to 10(-6) M had no effect on the enzyme activity. It appears therefore that the blood pressure potentiating effect of NPY is not restricted to alpha adrenoceptor stimulation with norepinephrine, but involves also the vasoconstrictor hormone angiotensin II. This NPY-induced potentiation does not seem to depend upon stimulation of alpha-2 adrenoceptors or inhibition of Na,K-adenosine triphosphatase.
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PMID:Effects of neuropeptide Y on the blood pressure response to various vasoconstrictor agents. 284 27

Neuropeptides are shown to exert a powerful influence on mnestic processes. They actively eliminate phenomena of electric-shock amnesia, the strongest agent here being arginine vasopressin, while derivatives of oxytocin, enkephalin, and melanostatin are active to a lesser degree. The selective effect on primary learning (ACTH4-7 and Leu-enkephalin) and on the consolidation and restoration of memory (vasopressin and oxytocin), and the presence of only antiamnestic properties (analog of the melanocyte-inhibiting factor) - all this suggests different mechanisms of action of these agents. Memory modulators act more strongly upon activated systems that are already prepared to receive the signal. A promising object for future study as a therapeutic antiamnestic factor is the long-term memory modulator arginine vasopressin.
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PMID:Comparative activity of memory-modulating neuropeptides before and after electric shock in white rats. 286 80

Oxytocin, vasopressin, melanostatin, bradykinin, LHRH-like peptide in different ways affected the spontaneous outflow and release of adrenaline and noradrenaline induced with central and peripheral nervous stimuli as well as with acetylcholine in the superfusate of the dog isolated inferior mesenteric ganglion.
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PMID:[Peptide modulation of spontaneous and evoked catecholamine release in the caudal mesenteric ganglion of the dog]. 287 2

The contractile effects of 19 factors on isolated human arterial segments at term pregnancy were quantified, and 14 contractile agents were similarly applied to preterm (23 to 35 weeks) umbilical arteries. Responses to potassium chloride were used to normalize the data. At comparison with the term vessel, the preterm artery contracted more to angiotensin II and arachidonic acid and was more sensitive to oxytocin. Contractions were greater in term arteries to vasopressin, norepinephrine, prostaglandin D2, and prostaglandin E2 but similar in both group of arteries to bradykinin, histamine, acetylcholine, and prostaglandin F2 alpha. Neuropeptide Y, linoleic acid, uridine triphosphate, and thrombin were ineffective. Hyperoxia inconsistently induced weak, short-lived contractions. Contractions to cooling manifested marked desensitization and tachyphylaxis. Serotonin was the only agonist that displayed the pharmacodynamic features most likely to be important for closure: potency, efficacy, and long duration of action (greater than 2.5 hours). It was postulated that cellular elements surrounding umbilical vessels are primary sources of vasoactive agents that are important to closure of the fetoplacental circulation at birth.
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PMID:Pharmacodynamic study of maturation and closure of human umbilical arteries. 291 87

The discovery of neuropeptides in mammalian nervous tissue has proceeded at an astonishing pace in recent years, encouraged by novel detection techniques which allow peptides to be extracted and sequenced before their biological activity has been determined (Mutt 1983; Sudcliffe et al. 1983). Most of these methods, poached from molecular biology, are nowadays reversing former trends which evolved either as a systematic search for factors known to control pituitary hormone release (vasopressin and oxytocin), for instance, or as an endeavour to find endogenous ligands for newly discovered receptors (the endorphins) (see Krieger 1983 for review). Neuropeptide tyrosine (NPY) has emerged as an important member of this new generation of peptides, not least because it is the most abundant and widely distributed in the mammalian brain. However, despite the considerable attention this peptide has attracted, we are far from understanding its functional significance. The following account traces the history of NPY and appraises some of the literature in an attempt to raise some speculation concerning its function; several reviews on this peptide already exist (Emson and de Quidt 1984; Solomon 1985; Allen and Bloom 1986; Gray and Morley 1986), Particular attention is paid to studies which have recently suggested that NPY might be involved with the pathogenesis of two neurodegenerative disorders, Huntington's chorea and Alzheimer's disease.
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PMID:The neuropeptide Y-immunoreactive neuronal system: discovery, anatomy and involvement in neurodegenerative disease. 295 70


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