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)

Since neuroimmunomodulation is brought about in part, at least, by secretion of pituitary hormones involved in stress and immune responses, we review briefly the hypothalamic control of the release of ACTH, growth hormone, and prolactin. The release of ACTH is controlled particularly by corticotropin-releasing factor (CRF), but vasopressin has intrinsic releasing activity and potentiates the action of CRF at both hypothalamic and pituitary levels. Oxytocin may even potentiate the action of CRF, but has little, if any, ACTH-releasing activity by itself. In addition, epinephrine may augment responses to the CRFs. In contrast, growth hormone is under dual control by growth-hormone-releasing factor (GRF) and somatostatin, and prolactin is under multifactorial control by a series of inhibitors and stimulators. Dopamine is accepted as a physiological prolactin-inhibiting factor (PIF), but probably GABA and possibly acetylcholine as well are PIFs. There is good evidence for a peptide PIF as well. There are a number of prolactin-releasing factors (PRFs) which include oxytocin, vasoactive intestinal polypeptide, PHI and TRH. Several other peptides can also release prolactin, including angiotensin II. In response to stress there is a complex interaction of peptides intrahypothalamically. CRF augments its own release by an ultra short-loop positive feedback, and there is negative ultra short-loop feedback of GRF and somatostatin. Vasopressin appears to augment CRF release as well as to act directly on the pituitary, and there are complex interactions of various peptides to influence prolactin and GH release.
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PMID:The role of brain peptides in neuroimmunomodulation. 347 67

GABAergic neuronal profiles in the supraoptic nucleus of the rat were immunohistochemically identified by using a purified GABA antibody with the peroxidase-antiperoxidase method. The localization of GABA-like immunoreactivity in nerve terminals on the neurosecretory neurons was examined electron microscopically. A few small GABAergic neurons were found inside the supraoptic nucleus while only a very few medium-sized ones were detected in the perinuclear zone. Intrinsic, non-GABAergic small neurons covered by GABAergic neuropil were also detected. The neuropil with GABAergic axo-somatic synapses evenly encompassed unlabeled neurosecretory perikarya throughout the supraoptic nucleus. The GABAergic system seems to inhibit both vasopressin and oxytocin cells. In this area, glia cells showed clear outlines of unlabeled somata around counter-stained nuclei. Blood capillaries in the supraoptic nucleus were only slightly covered with a GABAergic neuropil. Electron microscopic observations demonstrated the presence of GABAergic axo-somatic symmetrical and axo-dendritic asymmetrical synapses on the neurosecretory neurons. GABA-like immunoreactivity was localized on the membranes of microtubules and synaptic vesicles, on the external membranes of the mitochondria, and on the inner leaf of the presynaptic sites. Numerous pairs of non-immunoreactive synapses were arranged along these immunoreactive synapses.
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PMID:Immunohistochemical studies on the GABAergic system in the rat supraoptic nucleus using the PAP method with an application of electron microscopy. 355 72

The autoradiographic distribution of [3H]arginine vasopressin, [3H]spiperone, [3H]GABA, [3H]dihydroalprenolol and the peripheral-type benzodiazepine ligand [3H]Ro5-4864 were examined in the rat pituitary before and after pituitary stalk transection. Stalk transection produced dramatic changes in the cellular architecture of the pars nervosa. Glial fibrillary acidic protein, an astrocyte marker reported in pituicytes, increased after stalk transection, whereas neurofilament, a marker for neuronal innervation, was lost. These structural changes demonstrated a successful stalk transection, permitting interpretation of changes in the densities of several [3H]-ligands over the three lobes. [3H]Ro5-4864 binding was markedly increased, suggesting that this site was located on the pituicytes. Conversely [3H]spiperone and [3H]arginine vasopressin binding density over the pars nervosa decreased. In the mutant diabetes insipidus rat (Brattleboro), which lacks pituitary vasopressin, [3H]arginine vasopressin binding was undetectable in the pars nervosa. [3H]dihydroalprenolol and [3H]GABA binding sites were unchanged by the lesion. These results are discussed in terms of the occurrence of functional acceptors on pituicytes and their possible role in neurohydrophyseal secretions.
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PMID:Autoradiographic localization of peripheral benzodiazepine, dihydroalprenolol and arginine vasopressin binding sites in the pituitaries of control, stalk transected and Brattleboro rats. 378 75

Controversy exists as to the neural network whereby peripheral arterial baroreceptor information is transmitted to vasopressin (VP)-secreting neurons of the hypothalamic supraoptic nucleus (s.o.n.). In vivo electrophysiological studies in the rat were undertaken to characterize the selective depression of VP cell activity consequent to activation of peripheral baroreceptors. Electrical stimulation of the diagonal band of Broca (DB) in the rat evoked a similar selective inhibition of vasopressinergic neurons of the s.o.n. Local application of bicuculline, a GABA antagonist, abolished both the DB-evoked and baroreceptor-induced inhibition of VP-secreting neurons. In addition, recordings from DB neurons antidromically activated from the s.o.n. displayed an increase in firing consequent to baroreceptor activation, coinciding with the suppression of firing in s.o.n. VP neurons. These observations collectively indicate that an intrinsic GABA projection arising in the DB cell group selectively inhibits vasopressinergic neurons of the s.o.n. and that this pathway mediates peripheral arterial baroreceptor activity that influences the release of VP in the neurohypophysis. These data may be of critical importance in our understanding the etiology of those forms of experimental hypertension where abnormalities in central baroreceptor pathways have been implicated but not proven.
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PMID:Neurophysiology of a central baroreceptor pathway projecting to hypothalamic vasopressin neurons. 381 62

GABAergic agents microinjected into the nucleus tractus solitarius (NTS) influence blood pressure (BP) and plasma vasopressin (VP) levels. The direct-acting GABAergic agonist muscimol (3.75-160 pmol) microinjected bilaterally into the NTS of chloralose-anesthetized, paralyzed, ventilated rats increased BP without significantly altering heart rate. Similar results were obtained using the indirect GABA agonist nipecotic acid (10 nmol), a GABA uptake blocker. In contrast, blocking the action of GABA with bicuculline (5 pmol) elicited a small but consistent decrease in BP. Injections of the vehicle (artificial cerebrospinal fluid) into the NTS or GABAergic agents in an area lateral to the NTS did not alter BP. Unilateral injection of muscimol into the NTS did not elicit immediate pressor responses as did bilateral injections; unilateral muscimol injections following destruction of the contralateral NTS produced a pressor response similar to that seen following bilateral muscimol administration. Stimulation of GABA receptors within the NTS by either muscimol or nipecotic acid resulted in an increase in plasma VP levels. The elevated levels of plasma VP contributed to the pressor response elicited by stimulation of GABAergic receptors as evidenced by the decrease in BP observed following the intravenous administration of a VP pressor antagonist during the pressor response. These studies indicate that tonically active GABAergic mechanisms within the NTS influence BP and VP release, and provide further evidence that VP can be involved in cardiovascular responses elicited from the NTS.
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PMID:GABAergic mechanisms in nucleus tractus solitarius alter blood pressure and vasopressin release. 382 22

Systemic administration of the GABA antagonist picrotoxin 6.0 mg/kg i.v. elicited hypertension and a fall in sinus rate with a return to baseline levels in intact rats. Antagonists of GABA act in the supraspinal CNS to augment sympathetic outflow to the heart and vasculature. Therefore, in this study the spinal cord was transected prior to drug administration in order to eliminate sympathetically mediated effects. In spinal rats, picrotoxin 6.0 mg/kg evoked a biphasic sinus rate response characterized by an initial decrease followed by an increase above baseline sinus rate. Bilateral vagotomy or atropine pretreatment blocked sinus rate changes elicited by picrotoxin, demonstrating that these effects were vagally mediated. Midcollicular decerebration altered the biphasic sinus rate response by preventing the late rise but not the initial decrease in sinus rate. Infusion of another GABA antagonist, bicuculline, elicited a similar biphasic sinus rate response, although the time-course was shorter. Unexpectedly, picrotoxin or bicuculline administration in spinal rats caused an increase in mean blood pressure which was prevented by decerebration and different from that observed in intact rats with respect to time course. In spinal rats pretreatment with a vasopressin antagonist, D(CH2)5Tyr(Me)AVP, blocked the pressor response induced by picrotoxin infusion without altering the biphasic changes in sinus rate. These results suggest that, in the rat: (1) two GABAergic inhibitory mechanisms at different levels of the neuraxis exert opposite effects on cardiac vagal activity; and (2) GABA antagonists may elevate arterial pressure by a mechanism distinct from their previously described sympathoexcitatory effects.
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PMID:Biphasic effects of systemically administered GABA antagonists on cardiac vagal activity. 394 99

Neuropeptides are found in dense networks of neuronal perikarya, fibers and terminals within numerous brain regions. Among the more striking of these collections are sites within the central nervous system that are presumed to regulate either endocrine or autonomic function. A recent example of a neuropeptide which is likely to play a significant role in endocrine regulation is cortocotropin releasing factor (CRF). Immunohistochemical studies revealed that CRF immunoreactivity was found in many brain regions, including the paraventriculo-infundibular pathway. CRF released from nerve terminals belonging to this pathway presumably regulates ACTH release. Treatment of rats with reserpine depletes CRF as well as vasopressin from the external layer of the median eminence, suggesting tonic, monoaminergic inhibition of CRF and vasopressin containing neurons. CRF antisera were found which stain urotensin I immunoreactivity within the caudal neurosecretory system of fish. Numerous putative neurotransmitters impinge upon preganglionic sympathetic neurons within the intermediolateral cell column of the spinal cord. Preganglionic sympathetic neurons which innervate the adrenal medulla appear to have a specific input from somatostatin immunoreactive fibers. In addition, binding sites for serotonin and alpha-2 adrenergic ligands are more highly concentrated over sympathoadrenal neurons. Finally, the pancreatic islet contains peptide producing endocrine cells which possess several neuron-like properties. Some of these properties are reviewed, especially the finding that the insulin producing cells contain glutamate decarboxylase immunoreactivity, the biosynthetic enzyme for GABA. Further studies revealed that GABA agonists inhibit somatostatin release from islet cells.
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PMID:Peptidergic regulation in neuroendocrine and autonomic systems. 614 35

In the present study we investigated the effect of arginine-vasopressin (AVP) on responses induced in lateral septal neurons of the rat by iontophoretically administered excitatory and inhibitory amino acids and by synaptical stimuli delivered through fimbria-fornix (fi-fx) fibers. In the majority of the lateral septal neurons, iontophoretically applied AVP induced a marked increase in the excitatory responses to glutamate, aspartate, quisqualate and N-methyl-D-aspartate. The responses to excitatory amino acids frequently remained elevated several minutes after termination of the peptide administration. Inhibitory responses induced by GABA were not affected by AVP. The responsiveness of lateral septal single units to fi-fx stimuli was enhanced during iontophoretic administration of AVP. The enhanced responsiveness also appeared from experiments in which topically applied AVP induced a prolonged increase in the negative but not the positive wave of field potentials evoked in the lateral by fi-fx stimuli. The possible physiological significance of these findings is discussed.
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PMID:Arginine-vasopressin enhances the responses of lateral septal neurons in the rat to excitatory amino acids and fimbria-fornix stimuli. 614 88

Previous studies have demonstrated that intraventricular (i.v.t.) administration of low doses of GABA agonists reduced the central pressor effects of cerebrospinal fluid (CSF) made hypertonic with sodium (Na). The following studies were designed to determine if GABA agonists acted to decrease the pressor response of Na through inhibition of the vasopressin-dependent pressor component. Following pretreatment with vascular vasopressin antagonist, the pressor response of i.v.t. administered Na was reduced approximately 60%. Hypophysectomy produced a similar reduction in the pressor response elicited by hypertonic CSF. These results indicate that vasopressin contributed to approximately 60% of the pressor response of Na. In order to generate a vasopressin-dependent pressor response, the sympathetic nervous system was eliminated with ganglionic blockade by chlorisondamine. The increase in arterial pressure produced by i.v.t. injection of hypertonic CSF was augmented after ganglionic blockade compared to untreated rats. The augmented pressor effect of i.v.t. administered Na was markedly reduced by the vascular vasopressin antagonist or by hypophysectomy. Therefore, the pressor effect of Na after ganglionic blockade was caused almost entirely by the pressor actions of arginine-vasopressin (AVP). This AVP-dependent pressor effect of i.v.t. injected Na in rats subjected to ganglionic blockade was reduced by pretreatment with 100 micrograms of GABA or 50 ng of the GABA agonist muscimol. These doses of GABA and muscimol have previously been shown to reduce the pressor response of i.v.t. administered Na in untreated rats. Thus, pretreatment with low doses of GABA agonists reduced the pressor effect of Na in part through inhibition of the vasopressin component of the pressor response. GABA pretreatment also antagonized the increase in plasma AVP levels produced by i.v.t. administered hypertonic CSF.
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PMID:GABA agonists inhibit central sodium-induced vasopressin-dependent increases in arterial pressure. 648 42

A 24-year-old female with gastrointestinal disturbances, nausea and vomiting, had a convulsion with loss of urine and bitten lips on the 5th day of hospitalization. A significant decrease of sodium and potassium levels and lowered osmolality of the serum as well as urinary hyperosmolality permitted the diagnosis of the so-called syndrome of inappropriate antidiuretic hormone release (SIADH) of unknown aetiology, described by Schwartz-Bartter. Twice short tests for porphyria were negative; then the elevated porphyrin precursors collected in 24 h urine indicated the existence of an acute intermittent porphyria. A clinical follow-up and improvement were demonstrated by the EEG findings. Since animal experiments and pathohistological findings indicate that porphyrin metabolites such as delta-amino laevulinic acid and porphobilinogen may influence inhibitory and neurosecretory structures in central nervous tissue and interfere with GABA, cerebral hyperexcitability as well as disturbance of electrolytes may be explained. Finally, the question of whether the EEG changes are due to the significant electrolyte disturbances or are typical signs of acute intermittent porphyria is discussed.
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PMID:[EEG changes in a patient with acute intermittent porphyria and a Schwartz-Bartter syndrome (SIADH)]. 681 70


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