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)

Pituitary hormones profoundly influence behavior through direct actions on the brain. One of these behavioral effects is the attenuation of experimental amnesia. Traditionally, amnesia is considered as a "loss of memory." Memory comprises at least 2 stages: input (memory consolidation) and output (memory retrieval). Theoretically, disturbance of either aspect of memory may be the cause of amnesia. Also, it is possible that amnesia is based on a factor or factors not related to memory. Data and theories on amnesia in man were reviewed. Some salient features were mentioned: (1) amnesia can be induced by a variety of agents; (2) amnesia covers periods ranging from seconds to years; (3) amnesia gradients can be established; (4) amnesia is to a large extent reversible. From this survey, it seems possible that amnesia is not a homogeneous phenomenon and that even in one person a disturbance of both memory consolidation and memory retrieval may be produced by one and the same event. Animal studies in general have confirmed these conclusions. We have developed an animal model in order to study the effects of pituitary peptides on amnesia. This model is based on CO2-induced amnesia for a one-trial passive avoidance response in rats. This amnesia could be attenuated by treatment with ACTH-analogs 1 hour before the retrieval test. This anti-amnesic effect of ACTH-analogs was not dependent on the nature of the behavioral response or the amnesic treatment. The vasopressin-analog DGLVP similarly exerted an anti-amnesic effect when injected before the retrieval trial. In contrast to ACTH-analogs, however, it also reduced the amnesia when injected before acquisition. These results suggest that amnesia may comprise a "faulty-consolidation" and a "faulty-retrieval" component, which may be amended by different pituitary hormones. The study of the anti-amnesic activity of peptides therefore not only serves to characterize the nature of the behavioral effect of these peptides but may also prove to be helpful of the unraveling of processes involved in amnesia.
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PMID:Pituitary hormones and amnesia. 21 89

1. Propionate and other unbranched short-chain fatty acids, butyrate, pentanoate, hexanoate and octanoate were found to both stimulate and inhibit active sodium transport by the toad bladder, as measured by the short-circuit current (s.c.c.). 2. Stimulation alone followed addition of low concentrations of fatty acids (0.1-1.0 mM) to either the serosal or mucosal bathing medium; stimulation was also seen after an initial period of inhibition in response to higher concentrations (approx. 5 mM) of some compounds. 3. Inhibition alone followed addition of high concentrations (5-20 mM) of these compounds. The duration and magnitude of the inhibition varied with increasing concentration and chain length of the fatty acid, and was greater following mucosal addition than serosal addition. 4. The inhibitory effect of mucosal propionate increased with decreasing pH of the mucosal bathing medium. 5. Inhibition by the fatty acids was completely reversed upon removing the compound from the bathing medium, and stimulation characteristically followed. 6. In studies designed to evaluate the role of metabolism of the fatty acids in their mucosal inhibitory effects it was found that 14-c-labelled propionate, when added to the mucosal surface of the bladder, was converted to 14-CO2, and mucosal succinate and alpha-oxoglutaric acid at 20 mM inhibited the s.c.c. slightly. However, malonate did not interfere with inhibition by mucosal propionate and two non-metabolizable acids, dimethylpropionate and benzoate, induced inhibition (and no stimulation) of the s.c.c. 7. In the presence of an inhibitory concentration of fatty acid, the ability of the bladder to respond to added pyruvate was reduced in proportion to the reduction in the level of the s.c.c., whereas the natriferic response to vasopressin was largely intact. 8. We conclude that stimulation of sodium transport by propionate and other short-chain fatty acids is due to metabolism of the compounds and provision of energy to the sodium transport mechanism. The basis of the inhibition appears complex. It may in part depend on metabolism of the fatty acids and/or uncoupling of oxidative phosphorylation, with resultant reduction in net ATP production for the sodium transport mechanism. However, the inhibition may also be caused in part by a direct effect on the mucosal entry of sodium into the transporting epithelial cells.
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PMID:On the effects of propionate and other short-chain fatty acids on sodium transport by the toad bladder. 23 89

Active sodium transport and CO2 production were measured simultaneously in toad bladders mounted in membrane chambers. The rate of sodium transport was varied by changing the concentration of sodium in the mucosal bath (substitution with choline), by adding vasopressin, by adding metabolic substrates and by adding malonate, and the ratio of the change of sodium transport and CO2 production was determined Mean values for deltaNa/deltaCO2 (equiv/mole) were: Na in equilibrium choline 18.3 +/- 1.1; vasopressin 15.5 +/- 2.8; and pyruvate (corrected for the increment in "nontransport" CO2) 15.4 +/- 3.5. Based on previously determined values for the respiratory quotient (R.Q.), calculated mean values for deltaNa/deltaO2 ranged between 15.5 and 18.5 equiv/mole. It appears that basal metabolism does not contribute to metabolism supporting sodium transport when the rate of sodium transport is varied. "Transport" metabolism appears much more responsive to changes in the availability of endogenous and exogenous substrates than does "nontransport" metabolism. We conclude that "transport" and "nontransport" metabolism are functionally separated in the toad bladder.
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PMID:Interrelationships of sodium transport and carbon dioxide production by the toad bladder: response to changes in mucosal sodium concentration, to vasopressin and to availability of metabolic substrate. 40 60

Vasopressin-induced glucose release from the perfused livers of fed rats is diminished in the presence of insulin or following adrenal ablation. The reduced rate of glucose release following vasopressin treatment in the perfused livers of adrenalectomized rats was restored towards the control value by cortisol treatment in vivo. Vasopressin did not influence the total rate of fatty acid synthesis in the livers of fed rats perfused with medium containing glucose and two concentrations of lactate. The contribution of these precursors to hepatic fatty acid synthesis and CO2 production was similarly uninfluenced by vasopressin. Vasopressin casued a transient increase in the release of K+ by the perfused liver which was observed within 2 min of hormone administration. These results are discussed in relation to the possible mode of action of vasopressin in the liver.
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PMID:The control by vasopressin of carbohydrate and lipid metabolism in the perfused rat liver. 42 22

Experiments have been performed to examine the effects of activating the carotid body chemoreceptors and the arterial baroreceptors on the discharge of neurones within the hypothalamic supraoptic nucleus of the rat. Chemoreceptors were activated by intracarotid injection of 0.9% NaCl solution equilibrated with 100% CO2. The baroreceptors of the carotid sinus and aortic arch were activated by raising the blood pressure with an intravenous injection of phenylephrine. Chemoreceptor stimulation activated and baroreceptor stimulation inhibited the discharge of all the phasically discharging neurones tested. Neither stimulus had any consistent effect on non-phasically discharging neurones, although slight inhibition occasionally occurred. Anaesthesia of the carotid bifurcation abolished the effects of cardiovascular stimulation on the supraoptic neurones. Responses resumed when the anaesthesia wore off. However, the anaesthesia also seemed to alter the phasic pattern of discharge. The results are discussed with reference to the influence of the cardiovascular receptors upon the neurones in the supraoptic nucleus, and with reference to possible roles for the cardiovascular reflexes in control of vasopressin secretion.
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PMID:Effects of chemoreceptor and baroreceptor stimulation on the discharge of hypothalamic supraoptic neurones in rats. 47 26

Application of a foot shock during the acquisition trial of a one-trial passive avoidance task is associated with a rise in the concentration of serotonin in the hippocampus 24 h after conclusion of the acquisition trial. Carbon dioxide (CO2) induces amnesia for the passive avoidance response when administered immediately upon termination of the acquisition trial. In rats subjected to CO2 treatment following foot shock the rise in hippocampal serotonin is not observed 24 h later. The vasopressin analogue desglycinamide lysine vasopressin attenuates CO2-induced amnesia for the passive avoidance response when given prior to either the acquisition or the retrieval test (24 h after acquisition). This attenuation of the passive avoidance response is associated with a rise in the hippocampal serotonin concentration similar to the one observed in non-amnesic animals. It is suggested that a correlation exists between changes in hippocampal serotonin metabolism and the retrievability of the passive avoidance response.
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PMID:Parallel changes in behaviour and hippocampal serotonin metabolism in rats following treatment with desglycinamide lysine vasopressin. 55 78

1. Fotetal plasma vasopressin levels were measured by bio-assay in chronically catheterized sheep from 110 to 145 days gestation. 2. In foetuses in good condition resting circulating vasopressin concentrations were generally undetectable (less than 5 micromicron./ml.). In 15% of the samples low concentrations (5-10 micromicron./ml.) were observed. 3. Hypoxaemia in the foetus was caused by allowing the ewe to breathe 9% O2-3% CO2 in N2 for 1 hr. Plasma vasopressin levels rose in the foetus to 119 +/- 32 micromicron./ml., whereas the hormone levels in the ewe were not routinely increased. In the foetus, the rise in plasma vasopressin levels was significantly related to the fall in pH and Pa, O2 during the hypoxia. 4. In foetuses in which the cervical vagosympathetic trunks were cut, the rise in plasma vasopressin levels (to 48 +/- 25 micromicron./ml.) during hypoxaemia was less than in intact foetuses. The increase was related only to the fall in arterial pH and the regression coefficient was less than in intact foetuses. 5. During hypoxaemia arterial pressure rose and heart rate fell in the normal foetuses. The rise in arterial pressure was greatest when the plasma vasopressin concentration was highest. 6. Spontaneous episodes of hypoxaemia (Pa, O2 less than 15 mmHg) and/or acidaemia (pH less than 7.30) occurred in four intact foetuses and four foetuses in which the cervical vagosympathetic trunks were cut; all of the latter lambs died in utero. Plasma vasopressin levels were elevated and the concentrations were inversely related to arterial pH. 7. Intravenous infusions of vasopressin to foetuses increased plasma vasopressin levels to 6-202 micromicron./ml.; the rate of clearance of the hormone was three times that in adult ewes. There was a large increase in arterial pressure and bradycardia. The hypertensive effects of vasopressin were relatively much greater in the foetus than in adult ewes.
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PMID:Plasma vasopressin levels during hypoxaemia and the cardiovascular effects of exogenous vasopressin in foetal and adult sheep. 65 May 39

Since recent investigations have shown elevated urinary PGE2 and polyuria in hypokalemic animals which were reversed by PG synthesis inhibition with indomethacin, studies were undertaken to examine the effects of extracellular [K+] on renomedullary PG production in vitro. Slices of rabbit and human renal papilla were incubated in Krebs-Ringer HCO3- buffer, 95% O2-5% CO2, glucose 10 mM, HSA 4 gm/100 ml, for 30 min at 38 degrees C, with and without 1-14C-AA (10 micrometer). Measurments were made of total endogenous iPGE2 and iPGF2alpha production and radioactive AA leads to PGE2. In rabbit renal medulla values for iPGE2 (nmol/gm/30 min) were 252 +/- 20 at [K+] 0; 182 +/- 17 at [K+] 2.5 mEq/L; 163 +/- 18 at [K+] 5.5; and 129 +/- 17 [K+] 9.0 (p less than 0.005). iPGF2alpha was unaltered by changes in media potassium concentrations (6.8 +/- 0.9 nmol/gm/30 min at [K+] 0 and 6.2 +/- 0.8 at [K+] 9.0 MEq/L). In the human renal medulla iPGE2 was 9.5 +/- 1.6 nmol/gm/30 min at [K+] 0; 5.0 +/- 0.7 at [K+] 2.5 mEq/L; 5.3 +/- 0.3 at [K+] 5.5; and 4.6 +/- 1.0 at [K+] 9.0 (p less than 0.05). AA leads to PGE2 (nmol/gm/30 min) was 3.21 +/- 0.92 at [K+] 0; 2.47 +/- 0.57 at [K+] 2.5 mEq/L; 1.30 +/- 0.30 at [K+] 5.5; and 0.76 +/- 0.4 at [K+] 9.0 in rabbit medulla (P less than 0.005). It is postulated that direct stimulation of papillary PGE2 biosynthesis by low extracellular [K+] impairing the cAMP-generating response to vasopressin could represent the initial event in the pathogenesis of vasopressin-resistant polyuria.
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PMID:Renal biosynthesis of prostaglandin E2 and F2alpha: dependence on extracellular potassium. 71 2

When sodium transport (JNa) and CO2 production (JCO2) were measured simultaneously in the toad urinary bladder in the absence of electrochemical gradients under conditions of spontaneous variation of JNa, the curve of JNa on JCO2, phiJNa/phiJCO2, was found to be highly linear in an individual epithelium. However, no unique value appeared to characterize a population of bladders. In an effort to investigate the nature of this variation, phiJNa/phiJCO2 was examined under a variety of conditions. It was found that agents that affect sodium entry into the active transport pool, e.g. vasopressin and amiloride, or those that influence the energy-linked exit step, e.g. ouabain and insulin, have no effect on the phiJNa/phiJCO2. To investigate the possibility of the presence of a significant backleak from the serosal side into the cell, the sodium concentration was changed to 75 and 160 mM. Neither of these maneuvers influenced phiJNa/phiJCO2 or (JCO2)JNa=O. Furthermore, in the absence of mucosal sodium, ouabain had no effect on JCO2, suggesting that no significant recirculation is occurring. It is concluded that for each individual epithelium JNa is coupled to JCO2, and their ratios appear, within experimental error, to be invariant. It is suggested that sodium traverses the active transport pathway largely or entirely in one direction.
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PMID:Further studies on coupling between sodium transport and respiration in toad urinary bladder. 96 63

A patient with Shy-Drager syndrome exhibited a partial defect in antidiuretic hormone (ADH) release, and cluster breathing, an indication of pontomedullary respiratory center damage, with a normal CO2 response curve. This extends the spectrum of abnormalities associated with the degenerative disease of the central nervous system. The presence of a pontomedullary respiratory pattern without an impaired CO2 response curve suggests that neurons that determine respiratory rhythm function independently from those that function as chemoreceptors.
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PMID:Shy-Drager syndrome with abnormal respirations and antidiuretic hormone release. 125 43


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