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 role of Ca2+ in stimulation of the malate-aspartate shuttle by norepinephrine and vasopressin was studied in perfused rat liver. Shuttle capacity was indexed by measuring the changes in both the rate of production of glucose from sorbitol and the ratio of lactate to pyruvate during the oxidation of ethanol. (T. Sugano et al. (1986) Amer. J. Physiol. 251, E385-E392). Asparagine (0.5 mM), but not alanine (0.5 mM) decreased the ethanol-induced responses. Norepinephrine and vasopressin had no effect on the ethanol-induced responses when the liver was perfused with sorbitol or glycerol. In the presence of 0.25 mM alanine, norepinephrine, vasopressin, and A23187 decreased the ethanol-induced responses that occurred with the increase of flux of Ca2+. In liver perfused with Ca2+-free medium, asparagine also decreased the ethanol-induced responses, but norepinephrine and vasopressin had no effect. Aminooxyacetate inhibited the effects of norepinephrine, A23187, and asparagine. Regardless of the presence or absence of perfusate Ca2+, the combination of glucagon and alanine had no effect on the ethanol-induced responses. Norepinephrine caused a decrease in levels of alpha-ketoglutarate, aspartate, and glutamate in hepatocytes incubated with Ca2+. The present data suggest that the redistribution of cellular Ca2+ may activate the efflux of aspartate from mitochondria in rat liver, resulting in an increase in the capacity of the malate-aspartate shuttle.
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PMID:Ca2+-dependent activation of the malate-aspartate shuttle by norepinephrine and vasopressin in perfused rat liver. 289 18

A pharmaco-histochemical method for demonstrating the enzyme 4-aminobutyrate: 2-oxoglutarate transaminase was applied to the sections of the rat supraoptic nucleus region. The reactions of GABAergic interneurons and their relationship to neurosecretory neurons were studied. Medium-sized neurons heavily stained for transaminase were detected in the perinuclear zone just dorsal to the supraoptic nucleus. Neurons within the supraoptic nucleus were not stained. However, the perikarya of some neurosecretory neurons in the dorsal region of the supraoptic nucleus, as well as in discrete groups scattered throughout the nucleus; were surrounded by the granular reaction products. The results strongly suggest that these strongly positive neurons in the perinuclear zone send axons to the supraoptic nucleus, where they richly divide into many branches, which synapse on the perikarya of some vasopressin and oxytocin cells.
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PMID:4-aminobutyrate: 2-oxoglutarate transaminase-containing neurons in the perinuclear zone of the rat supraoptic nucleus. 309 48

Shortly after the injection of glucagon, epinephrine, norepinephrine, vasopressin, or angiotensin II into fasted rats, mitochondria isolated from their livers contained elevated concentrations of malate and oxidized citrate, alpha-ketoglutarate, and, in some cases, succinate more rapidly than mitochondria from fasted, control rats. The administration of tryptophan, lactate, or ethanol and refeeding of rats fasted 24 h result in similar elevations of mitochondrial malate concentration and oxidation of added substrates. Treatments that resulted in elevated mitochondrial malate resulted also in increased uptake of added citrate, alpha-ketoglutarate, pyruvate, and, in some cases, succinate. It is postulated that the well-documented effect of gluconeogenic hormones on mitochondrial oxidation of carboxylic substrates may be mediated by malate which not only yields oxalacetate to support the tricarboxylic acid cycle but also facilitates the transport of added substrates, and which is regenerated in the tricarboxylic acid cycle.
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PMID:The role of malate in hormone-induced enhancement of mitochondrial respiration. 395 65

Effect of Ca2+ and parathyroid hormone (PTH) on 14 CO2 production from certain metabolic substrates by isolated glomeruli of rat kidney were examined. Increasing calcium concentration in the incubation medium inhibited 14CO2 production from 14C-labeled alpha-ketoglutarate and succinate, stimulated 14CO2 production from [1-14C]glucose and [1-14C]glutamate, but was without effect on that from [6-14C]glucose. PTH in the presence but not in the absence of Ca2+ inhibited 14CO2 production from labeled alpha-ketoglutarate and glutamate but not from labeled glucose. Additions of cyclic AMP as well as hormonal agents known to act directly on the glomureli, such as histamine, epinephrine, prostaglandin E2, vasopressin, angiotensin II and insulin, did not alter 14 CO2 production from labeled alpha-ketoglutarate. These data show the presence of calcium-dependent inhibitory actions on PTH on oxidation of alpha-ketoglutarate and glutamate which may be independent of cyclic AMP. These metabolic effects of PTH may underlie the alteration in the glomerular ultrafiltration coefficient and glomerular filtration induced by the hormone.
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PMID:Effect of parathyroid hormone and calcium ions on substrate oxidation by isolated glomeruli of the rat. 611 29

Glucagon is able to diminish the net release of inorganic phosphate (Pi) occurring on incubation of isolated hepatocytes from 48-h-starved rats. Concomitantly the hormone increases the cellular Pi content. This is associated with a rise of Pi in the cytosolic fraction. Other hormonal effectors like phenylephrine, vasopressin and angiotensin II exert a smaller and transient effect as compared to glucagon. It is proposed that this increase in Pi availability to the mitochondria, by favouring substrate level phosphorylation at the succinyl-CoA synthetase step plays a role in the development of the metabolite pattern found in the mitochondrial matrix space after exposure of hepatocytes to glucagon or the above agents. With regard to the glutamate level this view is evidenced by the finding that its hormone-dependent decrease was inversely correlated to the respective increase in the cytosolic Pi concentration. Further evidence is provided by experiments with isolated mitochondria incubated under state-3 conditions at medium Pi concentrations corresponding to those metabolically active in the cytosolic compartment of control and glucagon-stimulated hepatocytes, being 2 mM and 3 mM, respectively. Increasing medium phosphate concentration from 2 mM to 3 mM caused a marked decrease in the level of succinyl-CoA and increased the rates of 2-oxoglutarate utilization and of malate and phosphoenolpyruvate production. Citrulline synthesis also was found to be stimulated at 3 mM Pi. Taken together our results suggest a role of Pi supply in mitochondrial actions of glucagon in intact hepatocytes. Moreover, they could contribute to a better interpretation of glucagon effects on isolated mitochondria from hormone-pretreated liver cells.
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PMID:Possible role of Pi supply in mitochondrial actions of glucagon. 614 21

In the hyperthyroid state, delta psi m, delta pHm and therefore delta p are increased in rat liver. An enhanced delta p accords with a higher energy output. The subcellular distribution of adenine nucleotides in different thyroid states does not reflect the driving force for mitochondrial adenine-nucleotide translocase (that is delta psi m). Therefore, a change in delta psi m cannot be solely responsible for the postulated stimulation of adenine-nucleotide transport by THs. This is also the case for the changes in delta pHm, and in the subcellular distribution of malate, 2-oxoglutarate and glutamate, that are observed under the influence of THs. T3 induces calcium influx into the liver cell within minutes. It increases respiration and gluconeogenesis with the same kinetics. Therefore, it is suggested that, as with glucagon and vasopressin, calcium is the mediator of these changes. The delta p is increased with T3 and glucagon treatment but not with vasopressin. The changes in delta psi m and delta pHm appear to be the result of the individual actions of these hormones on ATP-consuming and ATP-producing reactions. The delta psi p is only increased with T3 treatment. This is related to the different mechanisms of enhancing intracellular calcium that are used by vasopressin, glucagon and T3.
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PMID:Long-term and short-term changes in mitochondrial parameters by thyroid hormones. 822 13