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)

Thiol and glutathione (GSH) efflux across the sinusoidal plasma membrane in isolated perfused rat liver was stimulated by addition of hormones such as vasopressin, phenylephrine and adrenaline, whereas glucagon or dibutyryl cyclic AMP were without effect. Phenylephrine and adrenaline effects were sensitive to prazosin and phentolamine, respectively. The increase in thiol efflux was largely accounted for by an increase in GSH efflux. Thiol efflux and the hormone effects were abolished in GSH-depleted liver. Biliary GSH efflux was diminished upon hormone addition. The newly discovered hormone-dependence of GSH release across the sinusoidal plasma membrane may explain the known loss of GSH during conditions of experimental shock (traumatic or endotoxin) and stress and peripheral inflammation.
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PMID:Hepatic thiol and glutathione efflux under the influence of vasopressin, phenylephrine and adrenaline. 399 71

Recordings of SON single unit activity and systemic arterial blood pressure (B.P.) were taken from 10 rats while systemic infusions of angiotensin II (AII), 1-1000 ng/kg body weight/min in 7 steps, or phenylephrine, 1-100 ng in 3 steps were administered. The relationship between AII concentrations and neuronal activity was biphasic. Within the physiological range (1 ng to 100 ng) AII excited single units in a dose dependent manner, but it had little effect on B.P. At higher concentrations, B.P. rose and neuronal activity was decreased. Phenylephrine, however, did not excite neuronal activity. With increasing phenylephrine concentrations, B.P. rose and neuronal activity slowed. We conclude that increased B.P. may dampen the SON neuronal output by baroreceptor inhibition. Under physiological conditions, therefore, AII may serve to reinforce tonic vasopressin release while inhibiting vasopressin release at pressor doses. This further suggests a role for plasma AII as an important link of the renal-hypothalamic-hormonal feedback loop.
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PMID:Systemic angiotensin II, blood pressure and supraoptic neuronal activity. 404 78

Phenylephrine (2.0 microM) induces an alpha 1-receptor-mediated net efflux of Ca2+ from livers of fed rats perfused with medium containing physiological concentrations (1.3 mM) of Ca2+. The onset of efflux (7.1 +/- 0.5 s; n = 16) immediately precedes a stimulation of mitochondrial respiration and glycogenolysis. Maximal rates of efflux are observed between 35 s and 45 s after alpha-agonist administration; thereafter the rate decreases, to be no longer detectable after 3 min. Within seconds of terminating phenylephrine infusion, a net transient uptake of Ca2+ by the liver is observed. Similar effects were observed with vasopressin (1 m-unit/ml) and angiotensin (6 nM). Reducing the perfusate [Ca2+] from 1.3 mM to 10 microM had little effect on alpha-agonist-induced Ca2+ efflux, but abolished the subsequent Ca2+ re-uptake, and hence led to a net loss of 80-120 nmol of Ca2+/g of liver from the tissue. The administration at 5 min intervals of short pulses (90 s) of phenylephrine under these conditions resulted in diminishing amounts of Ca2+ efflux being detected, and these could be correlated with decreased rates of alpha-agonist-induced mitochondrial respiration and glucose output. An examination of the Ca2+ pool mobilized by alpha-adrenergic agonists revealed that a loss of Ca2+ from mitochondria and from a fraction enriched in microsomes accounts for all the Ca2+ efflux detected. It is proposed that the alpha-adrenergic agonists, vasopressin and angiotensin mobilize Ca2+ from the same readily depleted intracellular pool consisting predominantly of mitochondria and the endoplasmic reticulum, and that the hormone-induced enhanced rate of mitochondrial respiration and glycogenolysis is directly dependent on this mobilization.
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PMID:Calcium ion fluxes induced by the action of alpha-adrenergic agonists in perfused rat liver. 613 69

The effects of hypothyroidism on the hepatic alpha 1-receptor system were studied in isolated rat liver cells. Phenylephrine and vasopressin caused concentration-dependent activation of glycogen phosphorylase and release of 45Ca from 45Ca-loaded cells in either normal or thyroidectomized rats. However, the magnitude of both responses to phenylephrine was markedly suppressed after thyroidectomy and could be restored to near normal levels by in vivo treatment with 1-triiodothyronine (0.25 mg/kg/day) for 4 days. The potency of vasopressin to induce phosphorylase activation and 45Ca release was only slightly reduced by thyroidectomy. Binding of [3H]prazosin to putative alpha 1-receptors in purified liver plasma membranes revealed that the above changes were accompanied by a decrease in the density of binding sites from 567 +/- 51 fmol/mg of protein in controls to 326 +/- 51 fmol/mg in thyroidectomized rats and a return to 498 +/- 23 fmol/mg in thyroidectomized rats treated with 1-triiodothyronine. The affinity of binding sites for [3H]prazosin or for alpha-receptor agonists was the same in the three groups of rats and affinity for epinephrine was unaffected by the presence of guanyl-5'-yl imidodiphosphate (30-100 microM). From these findings, it appears that a reduction in the number of hepatic alpha 1-receptors is responsible for the selective decrease in alpha-adrenergic responses in the hypothyroid rat liver. These changes are opposite to those previously reported for hepatic beta-receptors.
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PMID:Decreased alpha 1-adrenoceptor responsiveness and density in liver cells of thyroidectomized rats. 627 32

Calcium efflux from rat liver perfused with nonrecirculating medium was observed at 1.4 s following 10(-6) M (-)epinephrine infusion, when the perfusate Ca2+ was 60 microM. Net calcium efflux was also seen in livers perfused with 1.3 microM Ca2+ at approximately 8 s. In isolated rat hepatocytes, phosphorylase, a cytosolic enzyme, was activated significantly at 3 s and maximally at approximately 15 s by phenylephrine (10(-5) M), epinephrine (10(-6) M), and vasopressin (10(-8) M). Hexose phosphates were elevated at between 3 and 6 s with vasopressin. Phenylephrine and vasopressin stimulated hepatocyte respiration relatively slowly. The effects took 10 s to become evident, were dependent on the presence of Ca2+, and were probably the result of increased total cellular reduced pyridine nucleotide observed at 5 s. The slowness of the increase in respiration indicates that it cannot be the cause of the Ca2+ mobilization, but is more likely to be a consequence of it. From these studies, it is proposed that, following binding of catecholamines to alpha 1-adrenergic receptors, Ca2+ is first mobilized from the plasma membrane resulting in an elevation of the free Ca2+ ion concentration in the cytosol (Charest, R., Blackmore, P. F., Berthon, B., and Exton, J. H. (1983) J. Biol. Chem. 258, 8769-8773) which stimulates phosphorylase kinase and, hence, phosphorylase. These events begin to occur within the first 2 to 3 s. Following this, the concentration of reduced pyridine nucleotide(s) increases at 5 s resulting in the stimulation of respiration seen at 10 s. These events occur more slowly than the mobilization of cell Ca2+ and activation of phosphorylase, and may be secondary to the rise in cytosolic Ca2+. The time at which mitochondrial Ca2+ decreases is not known, but it accounts for most of the Ca2+ mobilized.
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PMID:Time course of alpha1-adrenergic and vasopressin actions on phosphorylase activation, calcium efflux, pyridine nucleotide reduction, and respiration in hepatocytes. 630 7

The effects of phenylephrine (alpha 1 +) and prazosin (alpha 1 -) on water intake, diuresis, food intake and blood pressure were compared in conscious normal and diabetic insipidus (DI) Long Evans rats. The two drugs did not change the values measured on 24 hours in the two groups of animals (tables I and II). Phenylephrine induced a diuretic response in both normal and DI rats during the two first hours. Water intake was decreased in normal rats and increased in DI animals (fig. 1). Prazosin induced an antidiuretic effect in the two groups of animals, an increase in water intake in normal rats and a decrease in water intake in DI animals (fig. 2). Blood pressure was not changed in the two groups of animals two hours after injection. The comparison between the different results shows that the first changes induced by phenylephrine or prazosin were changes in diuresis. Since the two drugs act in a same way on the diuresis of normal and vasopressin--deprived rats, it is concluded that the neurohypophysial peptide is not involved in the variations of urinary volume induced by the alpha 1-adrenergic drugs.
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PMID:[Role of alpha 1 adrenergic receptors in water balance in the rat]. 631 53

1. A method is described for efficient and rapid isolation of viable hepatocyte suspensions from chick embryos in the last few days of incubation. 2. Although qualitatively similar, quantitative differences exist in the hormonal control of glycogen metabolism between embryonic and hatched chicks. 3. Glucagon and adrenaline activate glycogenolysis. 4. Insulin did not inhibit basal or glucagon-stimulated glycogenolysis. 5. Phenylephrine (an alpha-adrenergic agonist), angiotensin and vasopressin, all of which activate glycogen breakdown in rat liver through a Ca2+-dependent mechanism, were without effect on chick embryo hepatocytes.
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PMID:Hormonal regulation of glycogen metabolism in hepatocyte suspensions isolated from chicken embryos. 680 8

Phenylephrine, vasopressin and the bivalent cation ionophore A23187 mobilized Ca2+ normally, but failed to activate phosphorylase, in hepatocytes from gsd/gsd rats with a deficiency of liver phosphorylase b kinase. These data provide strong evidence that phosphorylase b kinase is the site of action of the Ca2+ mobilized intracellularly during alpha 1-adrenergic activation of phosphorylase in liver cells.
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PMID:Alpha 1-Adrenergic stimulation of Ca2+ mobilization without phosphorylase activation in hepatocytes from phosphorylase b kinase-deficient gsd/gsd rats. 694 57

The effects of insulin on alpha-agonist (phenylephrine)- and [Arg8]vasopressin-induced Ca2+ and glucose release and mitochondrial Ca2+ fluxes in isolated perfused rat livers were examined. Insulin (6 nM) inhibited the ability of phenylephrine (1 and 0.5 microM) to elicit Ca2+ and glucose release, whereas it was without effect on vasopressin (10 and 2.5 nM) actions. Correspondingly, insulin inhibited the action of phenylephrine to induce a stable increase in mitochondrial Ca2+ uptake, but it did not affect the alteration caused by vasopressin. Phenylephrine and vasopressin caused transient increases in hepatocyte respiration. Insulin inhibited the effect of phenylephrine on this parameter, but not that of vasopressin. Insulin added alone did not alter any of the above parameters. It is concluded from these data that insulin does not alter cellular Ca2+ fluxes and respiration themselves, but selectively inhibits alpha-adrenergic stimulation of these processes. It is proposed that insulin acts either to inhibit binding of alpha-agonists to their specific plasma-membrane receptors or to alter generation and/or degradation of the putative alpha-adrenergic 'second messenger'. If this latter possibility is the case, then the alpha-adrenergic 'second messenger' must be different from the 'second messenger' of vasopressin.
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PMID:Insulin inhibition of alpha-adrenergic actions in liver. 703 Mar 20

Phenylephrine (1.5 x 10(-6) M) administered to perfused livers from fed rats gave rise to a rapid, parallel increase in oxygen uptake and glucose output. The time of onset for oxygen uptake was 9.9 +/- 0.4 s following phenylephrine administration, and immediately preceded glucose output which occurred at 11.6 +/- 0.5 s. Near-maximal effects were observed 50 s following alpha-agonist treatment. Both responses appear to be mediated by alpha- 1-adrenergic receptors. The mitochondrial respiratory chain blockers antimycin A and rotenone, inhibited the alpha-agonist-induced oxygen uptake and glycogenolytic responses at inhibitor concentrations similar to those required to block uncoupler-stimulated respiration in the intact perfused liver. Oligomycin and carboxyatractyloside also inhibited the phenylephrine-induced respiratory response. Vasopressin (1 milliunit/ml), and angiotensin II (6 x 10(-9) M) had effects similar to phenylephrine in the perfused liver which also were prevented by the prior administration of antimycin A and rotenone. In contrast, glucagon-induced (10(-8) M) glycogenolysis proceeded in the absence of large changes in respiration, was slower in onset (26.1 +/- 4.2 s following hormone administration), and was not inhibited by mitochondrial respiratory blockers. These data indicate that glycogenolysis induced by alpha-adrenergic agonists, vasopressin, and angiotensin II is associated with a large increase in mitochondrial respiration, that may play a role in a general, as yet undefined mechanism whereby these agents stimulate glycogenolysis in rat liver.
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PMID:Studies on alpha-adrenergic-induced respiration and glycogenolysis in perfused rat liver. 705 51


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