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)

The effects of streptozotocin-induced diabetes mellitus on the activity of discrete regions of the brain were studied with histochemical localization and photodensitometric quantification of the metabolic enzyme, hexokinase. Two weeks after a single injection of streptozotocin (65 mg/kg, i.p.), plasma glucose and osmolarity levels were elevated, and plasma sodium concentrations were depressed. These changes were reversed in diabetic rats treated with insulin. Accompanying these symptoms of diabetes were significant increases in hexokinase activity in the magnocellular division of the paraventricular nucleus of the hypothalamus (mPVH, 12.1%), the medial subdivision of the nucleus of the tractus solitarius (mNTS, 15.5%), and the commissural subdivision of the NTS (cNTS, 10.9%). An increase, though just below the level of significance, was also observed in the supraoptic nucleus of the hypothalamus (SON, 11.5%). The increases in hexokinase activity were completely reversed in the cNTS (and SON) and only partly reversed in the mPVH and mNTS of insulin-treated diabetic rats. No changes in hexokinase activity were seen in the subfornical organ, medial preoptic area, parvocellular division of the PVH, locus coeruleus, or dorsal motor nucleus of the vagus of diabetic rats. These results reinforce the idea that the brain is not exempt from changes associated with diabetes mellitus and suggest that metabolic alterations in the mPVH (and SON) and two divisions of the NTS are likely related to changes in vasopressin production and blood volume, respectively.
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PMID:Alterations in brain hexokinase activity associated with streptozotocin-induced diabetes mellitus in the rat. 222 10

This paper describes the vasopressin (VP) and oxytocin (OXT) immunoreactive structures in the brain and upper spinal cord of the adult male and female Macaca fascicularis. Immunocytochemistry following intraventricular application of colchicine displayed VP neurons in the diagonal band of Broca (DBB), bed nucleus of the stria terminalis (BST), medial amygdaloid nucleus, dorsomedial hypothalamic nucleus, area of the locus coeruleus (LC), solitary tract nuclei (NTS), and the dorsal horn of the cervical spinal cord in addition to those known to exist in the paraventricular, supraoptic, and suprachiasmatic hypothalamic nuclei. Furthermore, a dense accumulation of VP fibers was observed in areas such as the DBB, medial septum, BST, amygdala, hippocampus, ventral tegmental area, periaquaductal gray, dorsal and ventral raphe, area of Forel, LC region, parabrachial nuclei, and NTS. The lateral septum and lateral habenula displayed no and very few VP fibers, respectively. No extrahypothalamic OXT neurons were found in the brain of this macaque monkey. Dense concentrations of OXT fibers were demonstrated in the amygdala, NTS, and marginal layer of the cervical spinal cord. No sexual dimorphism was found in this primate VP or OXT system. The results show a distribution of the central VP and OXT systems in this primate which is quite different from that in the rat. However, in various aspects it agrees with current data on the VP and OXT systems of the human brain. The present results suggest, therefore, that this monkey might serve as a better model for the human VP system than the rat.
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PMID:Vasopressin and oxytocin systems in the brain and upper spinal cord of Macaca fascicularis. 277 7

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

The roles of putative central neurotransmitters in the control of blood pressure have been reviewed with respect to the cardiovascular functions of individual nerve pathways in the medulla oblongata and spinal cord. Vasomotor activity of sympathetic preganglionic neurones originates from spinally-projecting neurones in the ventrolateral medulla which may include adrenaline neurones of the C1 group and serotonin neurones in the lateral B1 and B3 groups. Other bulbospinal monoamine nerves may modulate vasomotor activity at the spinal level, but the mechanism of this modulation is controversial. Evidence for two descending sympatho-inhibitory pathways has emerged: a noradrenergic projection from the A5 cell group and a serotonergic projection from the medullary raphe (medial B1 and B2 groups). The vasomotor influence of other bulbospinal pathways is unclear. Baroreflex control of blood pressure is mediated through the solitary tract nucleus (NTS). L-Glutamate and substance P are considered as candidates for transmitters in baroreceptor afferents to the NTS. Transmitters in efferent nerves relaying baroreflex activity from the NTS to cardiovagal motoneurones, medullary vasomotor neurones or sympathetic preganglionic neurones have not been identified but the monoamine transmitters present in the NTS appear to modulate baroreflexes. Noradrenaline and serotonin nerve endings may facilitate the vasodepressor component of the baroreflex while adrenaline nerves possibly inhibit the cardiovagal mechanism. Enkephalins and vasopressin act in the NTS to raise blood pressure and nerves containing these neuropeptides may constitute important links in reciprocal cardiovascular pathways between the lower brainstem and hypothalamus.
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PMID:Blood pressure control by neurotransmitters in the medulla oblongata and spinal cord. 286 Jan 49

The neurones in the supraoptic and paraventricular nuclei (SON and PVN) which secrete vasopressin are separate from those which secrete oxytocin and are distributed in different parts of the nuclei. They may be distinguished electrophysiologically by a characteristic phasic pattern of firing. A selective afferent neural input to these neurones would provide a mechanism for the release of vasopressin independently of oxytocin in response to appropriate physiological stimuli. Release of vasopressin is controlled by changes in blood volume or pressure ('volume control') and in plasma osmolality ('osmotic control'). Stimuli involved in volume control such as haemorrhage, hypotension and carotid occlusion cause vasopressin to be released into the circulation with little or no detectable oxytocin. An osmotic stimulus releases vasopressin alone in some species but not apparently in the rat in which both hormones are released. Volume control is mediated reflexly by peripheral receptors in the cardiovascular system. Activation of baro- and stretch receptors results in inhibition, and activation of chemoreceptors in stimulation, of release. Afferent impulses from these receptors are conveyed in the vagi and carotid sinus nerves to the NTS on the dorsal surface of the brain stem. All afferent impulses to the NTS are excitatory. It follows that the afferents from chemoreceptors must stimulate an excitatory, and those from baro- and stretch receptors an inhibitory, projection from the NTS to the vasopressin-secreting cells in the SON and PVN. Two alternative models are presented of the neural pathways and transmitters involved. The model of Fig. 2 shows an excitatory relay through a cholinoceptive area on the ventral surface of the brain stem which has been termed the 'nicotine-sensitive area' because topical application of nicotine to this area in the cat released vasopressin without oxytocin. An inhibitory relay is shown through the A1 group of noradrenergic neurones on the ventral surface which selectively innervate the vasopressin-secreting neurones in the SON. This model implies an inhibitory role for noradrenaline acting on beta- or alpha 2-receptors. However the most recent investigations suggest an excitatory, rather than inhibitory, function of the A1 noradrenergic neurones involving alpha 1-receptors. This is the basis of the model in Fig. 3. The A1 neurones project either directly to the SON and PVN or indirectly through the lateral preoptic nucleus which lies in close proximity to the SON. The nicotine-sensitive area may be coincident with the A1 group of noradrenergic neurones.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Control of release of vasopressin by neuroendocrine reflexes. 290 66

We have reported that microinjection of angiotensin II (ANG II) into the nucleus tractus solitarius of urethan-anesthetized normotensive rats produces an increase in mean arterial pressure (MAP) over the dose range 50-500 pmol. The effect in spontaneously hypertensive rats (SHR) is now reported. Over the range 100-500 pmol SHR exhibit increases in MAP and heart rate greater than Wistar-Kyoto or Sprague-Dawley rats. SHR did not exhibit exaggerated responses to intravenous phenylephrine, suggesting a central site of increased responsiveness to ANG II. We also found depressor effects in Sprague-Dawley at lower doses (0.1 and 1 pmol). The decreases in MAP were extremely variable and not dose related. A selected dose of additional neuropeptides identified in the NTS was tested. Somatostatin, bradykinin, and vasoactive intestinal peptide (0.5 nmol) were without cardiovascular effects. Oxytocin and vasopressin, however, produced significant increases in MAP. Substance P produced a very small but significant increase in heart rate and MAP. Interaction between the vasopressin and ANG II pressor effects was studied, and each proved to be independent.
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PMID:Neuropeptide action in nucleus tractus solitarius: angiotensin specificity and hypertensive rats. 293 Oct 31

In urethane-anesthetized rats, injections of 50 pmol of arginine-vasopressin (AVP) or thyrotropin-releasing hormone (TRH) into a lateral cerebral ventricle (i.c.v.) elicit short-latency increases in blood pressure. i.c.v. injection of 50 pmol of the AVP antagonist, d(CH2)5Tyr(Me)AVP, but not of the vehicle (artificial cerebrospinal fluid; a CSF), abolished the pressor action of i.c.v. AVP. The AVP antagonist did not antagonize the TRH-induced pressor responses. In another group of rats, a monopolar stainless-steel electrode was positioned stereotaxically in the paraventricular nucleus (PVN) and pressor responses were elicited by electrical stimulation of the PVN. Micro-injection of 1 nmol of the AVP antagonist, but not of aCSF alone, into the nucleus tractus solitarius/vagal area (NTS/VA), reduced PVN-stimulated pressor responses to 26 +/- 6% of control and stimulation-induced tachycardia to 37.3 +/- 9.0% of control. These studies indicate that the pressor and heart-rate responses to PVN stimulation may be mediated, in part, via AVP receptors in the NTS/VA.
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PMID:Vasopressin antagonist in nucleus tractus solitarius/vagal area reduces pressor and tachycardia responses to paraventricular nucleus stimulation in rats. 392 90

Somatostatin (SRIF) and vasopressin (AVP) were measured in hypothalamic and extrahypothalamic areas in normotensive Wistar-Kyoto (WK) and in spontaneously hypertensive, adult rats (SRH) under control conditions and after acute immobilization stress. Hypothalamic areas included the median eminence (ME) and the periventricular, suprachiasmatic, paraventricular, supraoptic, ventromedial and dorsomedial nuclei. Extra-hypothalamic areas included the striae medullaris, striae terminalis (N. Interst.), locus coeruleus, central gray, Areas 1 and 2 (NTS), and circumventricular organs. Under basal conditions, SHR and WK rats did not differ in their content of SRIF and AVP for most areas examined. After acute stress, however, striking differences were found in peptide content. Somatostatin content was not changed in SHR, but was significantly decreased in most areas in WK rats. On the contrary, generalized increases in AVP content were found in SHR after stress, with no changes in WK animals. An exception was the ME, which showed a decrease in peptide levels in both groups of rats. These results suggest that both hypothalamic and extra-hypothalamic AVP and SRIF are involved in the central stress response. The different changes in peptide levels observed for SHR and normotensive rats after acute stress further support the hypothesis of a role of both AVP and SRIF in central regulation of cardiovascular function.
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PMID:Changes in brain somatostatin and vasopressin levels after stress in spontaneously hypertensive and Wistar-Kyoto rats. 610 6

Intracerebroventricular (i.c.v.) infusions of angiotensin II (AII) reliably induced c-fos expression in the supraoptic (SON) and paraventricular (PVN) nuclei, as well as other areas of the basal forebrain including the OVLT, subfornical organ (SFO), and bed nucleus (BNST). Double-labelling showed that AII-induced c-fos was observed in both vasopressin (AVP-) and oxytocin (OXY)-containing neurons of the SON and PVN in male rats. Allowing rats to drink water after AII infusions suppressed c-fos expression both AVP- and OXY-stained magnocellular neurons. Intragastric infusions of water were also effective, showing that oro-pharyngeal stimuli were not critical. Maximal suppression occurred in rats in whom water had been infused intragastrically about 5 min before i.c.v. AII infusions, suggesting that changes in osmolarity were responsible. i.c.v. AII also induced c-fos expression in a number of brainstem structures, including the solitary nucleus (NTS), lateral parabrachial nucleus (LPBN), locus coeruleus (LC), and the area postrema (AP). These results indicate that AVP and OXY-containing neurons in the magnocellular parts of the SON and PVN alter their immediate-early gene response to AII after water intake, and that this does not depend upon oro-pharyngeal factors. Furthermore, AII can induce c-fos expression in a number of brainstem nuclei associated with autonomic function, and these do not respond to water intake.
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PMID:Regional suppression by water intake of c-fos expression induced by intraventricular infusions of angiotensin II. 782 Jun 57

Rats with chronic nucleus of the solitary tract lesions (NTS-X) drink water and release vasopressin (VP) in response to reduced blood volume despite an absence of neural signals from cardiac and arterial baroreceptors. The present study determined whether rats with NTS-X have a greater sensitivity to circulating ANG II, which may contribute to the drinking and VP responses to hypovolemia. In conscious control rats and rats with NTS-X, ANG II was infused intravenously for 1 h at 10, 100, or 250 ng. kg(-1). min(-1). At the two higher doses, ANG II stimulated more water intake with a shorter latency to drink in rats with NTS-X than in control rats. In contrast, infusion of ANG II produced comparable increases in plasma VP in the two groups. At the two higher doses, ANG II produced an enhanced increase in arterial pressure (AP) in rats with NTS-X, and the bradycardia seen in control rats was reversed to a tachycardia. Infusion of hypertonic saline, which did not alter AP or heart rate, produced comparable drinking and VP release in the two groups. These results demonstrate that chronic NTS-X increases the dipsogenic response of rats to systemic ANG II but has no effect on ANG II-induced VP release or the osmotic stimulation of these responses.
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PMID:Nucleus of the solitary tract lesions enhance drinking, but not vasopressin release, induced by angiotensin. 1089 87


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