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)

1. The effect of intravenous infusions of various ions on the antidiuretic action of antidiuretic hormone has been studied in rats.2. Lithium (13 mmol/l.) reversibly inhibits the antidiuretic responses. Similar concentrations of potassium, rubidium, strontium, magnesium, choline and calcium do not. Lithium has a similar effect on the antidiuretic activity of oxytocin.3. The inhibition is not simply related to blood nor whole body lithium concentrations.4. Lithium (2 mmol/l.) in contact with the serosal surface also inhibits the transport of water facilitated by either 0.5 U/l. antidiuretic hormone or 1.1 mmol/l. cyclic adenosine monophosphate in the isolated toad bladder.5. Choline (2 mmol/l.) on the serosal surface also inhibits the transport of water facilitated by vasopressin in the toad bladder.
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PMID:Some aspects of the inhibition of the action of antidiuretic hormone by lithium ions in the rat kidney and bladder of the toad Bufo marinus. 435 11

Addition of vasopressin to rat hepatocytes prelabeled with myo-[2-3H]inositol resulted in a very rapid decrease [3H]phosphatidylinositol 4,5-bisphosphate (Ptd-Ins-4,5-P2) which was paralleled by increases of up to 3-fold in the levels of [3H]inositol trisphosphate (Ins-P3) and [3H]inositol bisphosphate (Ins-P2). Increases of [3H]inositol phosphate (Ins-P) were not detected until about 5 min after hormone addition. These data indicate that the major pathway for hormone-induced lipid breakdown in liver is through a phosphodiesterase for PtdIns-4,5-P2 and that decreases of phosphatidylinositol are a secondary result of increased PtdIns-4,5-P2 resynthesis. Using the fluorescent Ca2+ indicator Quin 2, cytosolic free Ca2+ increased from 160 nM to about 400 nM after vasopressin addition to hepatocytes and preceded the conversion of phosphorylase b to a. Half-maximal and maximal increases of cytosolic free Ca2+ and phosphorylase a activity were observed at 0.2 and 1 nM vasopressin, respectively. The dose-response curve for the initial rate of cytosolic free Ca2+ increase was very similar to those obtained for the initial rates of Ins-P3 production and PtdIns-4,5-P2 breakdown. Pretreatment of hepatocytes with Li+ caused a 3--4-fold potentiation of vasopressin-induced elevations of Ins-P, Ins-P2, and Ins-P3, with half-maximal effects at 0.5, 1, and 5 mM, respectively. The calculated maximal concentrations of Ins-P3 in cells treated with 20 nM vasopressin were 10 and 30 microM, respectively, without and with Li+. Lithium did not affect the initial rate of inositol polyphosphate production or Ca2+ mobilization. The increase of Ins-P3 which correlated with peak cytosolic free Ca2+ elevation was about 0.6 microM. In a saponin-permeabilized hepatocyte preparation, Ins-P3 (1 microM) caused Ca2+ release from a vesicular, ATP-dependent Ca2+ pool. The data presented here suggest that Ins-P3 may be a second messenger for the mobilization of intracellular Ca2+ by hormones in liver.
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PMID:Relationship between inositol polyphosphate production and the increase of cytosolic free Ca2+ induced by vasopressin in isolated hepatocytes. 632 42

Light and electron microscopy were used to study the effects of a lithium-supplemented diet on renal structure in the rat. At the end of a 7-week experimental period serum lithium levels were 1.14 +/- 0.20 mM. Lesions consisting of groups of dilated tubules were found in the immediate vicinity of the interlobular arteries in all experimental animals. These tubules were identified as the connecting tubule or the initial portion of the collecting tubule. The epithelium of these tubules was generally flattened but was punctuated by markedly swollen epithelial cells. PAS-positive deposits found in both types of cells were identified as glycogen. Electron microscopy revealed considerable lithium-induced damage in the swollen cells including increased numbers of mitochondria, many of which were swollen or otherwise damaged, dilated cisternae of endoplasmic reticulum and vacuolization of the apical cytoplasm. The flattened cells of these tubules were similar to the dark or intercalated cells of normal collecting tubules. Some detachment of epithelial cells from their basement membrane was evident in these tubules. Damage was less severe in distal convoluted tubules. Lithium-induced changes were not observed in glomeruli, proximal tubules or ascending thick limbs of Henle. In medullary collecting tubules damage was less severe than in cortical collecting tubules, but detachment of epithelial cells was a common finding. The interstitial tissue of the papilla exhibited histochemical and ultrastructural changes consistent with lithium blockade of the action of antidiuretic hormone. The ultrastructural damage to cortical tubules is similar to that found in patients receiving therapeutic lithium for long periods of time. The anatomic sites of lithium-induced pathology correspond to the location of lithium-induced pathophysiology.
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PMID:Effects of lithium on the structure of the rat kidney. 686 74

The collecting ducts in papillae taken from normal rats have a measurable increase in diffusional tritiated water (THO) permeability with ADH 5 mu unit/ml and this increase is maximal with antidiuretic hormone (ADH) 100 mu unit/ml added to media. The presence of plasma from rats pretreated with lithium to make them polyuric inhibited the response to ADH. The lowest concentration of ADH that caused a measurable increase in diffusional water permeability was 50 mu unit/ml and the increase was maximal with ADH 2000 mu unit/ml. The maximum response to ADH did not differ whether plasma from control or lithium pretreated rats was used. However, the dose-response curve to ADH was shifted to the right by the plasma from lithium-pretreated rats. Lithium added to the plasma from control rats did not alter the response to ADH. It is proposed that lithium given to rats causes a circulatory factor to be produced that inhibits in a competitive fashion the response of the collecting duct to ADH. Such an effect would explain many features of the impairment of water excretion associated with lithium use.
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PMID:The mechanism of polyuria in rats pretreated with lithium studies by in vitro microperfusion. 687 33

The relation between functional and structural renal changes induced by lithium was studied in rats during long-term treatment and after withdrawal of lithium. Administration of LiCl in the diet for up to 21 weeks caused marked polyuria associated with a significant lowering of renal concentrating ability assessed by dehydration and vasopressin tests. Plasma creatinine and plasma urea were not significantly changed by the treatment. Upon withdrawal of lithium water intake and concentrating ability were normalized within 4--8 weeks. Lithium caused focal light microscopic changes in the distal convoluted tubule and the collecting duct, consisting of nuclear and cellular polymorphism and, after prolonged treatment, dilatation of tubular lumens with tubular cell atrophy. These changes appeared later than the concentrating defect and persisted when lithium was withdrawn after prolonged treatment. No significant correlation was found between the degree of tubular changes and water intake or concentrating ability. It is concluded that the reversible diabetes insipidus induced by lithium in rats cannot be explained directly by the light microscopical changes observed in the distal part of the nephron, although the structural changes may be secondary to the polyuric state induced by lithium.
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PMID:Functional and structural changes in the rat kidney by long-term lithium treatment. 707 12

Lithium, a widely used treatment for bipolar affective disorders, often causes nephrogenic diabetes insipidus. The effect of chronic lithium therapy on the expression of the vasopressin-regulated water channel Aquaporin-2 (AQP2) in rat kidney was examined. Membranes were prepared from inner medulla of one kidney from each rat, while the contralateral one was fixed for immunofluorescence and immunoelectronmicroscopy. Immunoblotting revealed that lithium treatment reduced AQP2 expression dramatically, to 31 +/- 8% after 10 d and to 4 +/- 1% after 25 d, coincident with development of severe polyuria. Immunofluorescence and immunogold quantitation confirmed the lithium-induced decrease in AQP2 expression (from 11.2 +/- 1.0 to 1.1 +/- 0.2 particles/microns 2). The downregulation was only partly reversed by return to lithium-free diet for 1 wk (40 +/- 8% of control). Furthermore, immunoblotting and immunogold quantitation revealed that 2 d of thirsting or 7 d of dDAVP treatment, in the continued presence of lithium, increased AQP2 expression by six- and threefold, respectively, coincident with increased urinary osmolality. Thirsting increased AQP2 immunolabeling mainly of vesicles, whereas dDAVP caused accumulation of AQP2 predominantly in the subapical region and plasma membrane. Thus, lithium causes marked downregulation of AQP2 expression, only partially reversed by cessation of therapy, thirsting or dDAVP treatment, consistent with clinical observations of slow recovery from lithium-induced urinary concentrating defects.
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PMID:Lithium-induced downregulation of aquaporin-2 water channel expression in rat kidney medulla. 753

Animal studies have shown increased fluid absorption from the peritoneal cavity following intraperitoneal (ip) vasopressin. Lithium is known to antagonize vasopressin effects on fluid absorption in kidney distal nephrons. The aim of the present study was to see whether lithium-containing exchanges increase the ultrafiltration rates (UF) during peritoneal dialysis (PD) in rats. PD was carried out in 6 Sprague-Dawley rats with 1.5% dextrose-containing PD solution using 15-ml volumes. Each exchange (ex) took 1 min for inflow, 4 mins for outflow and 25 mins for dwell. All rats underwent 9 consecutive half-hourly exs. During exs 4-6 lithium carbonate 2.5 mM was added to the PD solution. During lithium-containing exs significant increases in the glucose absorption rates (3.9 +/- 7.8 vs 37.5 +/- 8.1 mg/ex; p = 0.025) were associated with significant reductions in the UF (3.03 +/- 0.25 vs 1.78 +/- 0.12 ml/ex; p = 0.005). In conclusion, the isolated increase in glucose absorption without increases in the dialysate protein concentration with ip lithium, may suggest either a selective increase in size of the pores with a mean dimater near that of the glucose molecule or enhanced lymphatic absorption. ip lithium did not increase the UF in a rat model of PD.
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PMID:Lithium carbonate decreases ultrafiltration rates in an experimental model of PD. 774 15

Lithium lengthens the free-running period of circadian rhythms in a wide variety of organisms. The object of the present study was to examine the effects of lithium treatment on free-running activity rhythms in suprachiasmatic nuclei lesioned (SCN-X) hamsters that had recovered circadian rhythmicity following transplantation of fetal anterior hypothalamic grafts containing the suprachiasmatic nuclei (SCN). The animals were housed individually in cages equipped with running wheels, and locomotor activity was monitored using a computer-based data acquisition system. At the end of the behavioral tests, animals were anesthetized and perfused. Brain sections were immunostained for vasoactive intestinal peptide (VIP) and vasopressin-associated neurophysin (NP) to evaluate the extent of the lesion and the presence of a functional graft. In both intact and in SCN-X grafted animals, lithium lengthened the period of free running activity without affecting the amount of activity or the precision of the rhythm.
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PMID:Lithium lengthens the period of circadian rhythms in lesioned hamsters bearing SCN grafts. 825 Oct 24

Prolonged hypokalemia causes vasopressin-resistant polyuria. We have recently shown that another cause of severe polyuria, chronic lithium therapy, is associated with decreased aquaporin-2 (AQP2) water channel expression (Marples, D., S. Christensen, E.I. Christensen, P.D. Ottosen, and S. Nielsen, 1995. J. Clin. Invest., 95: 1838-1845). Consequently, we studied the effect in rats of 11 days' potassium deprivation on urine production and AQP2 expression and distribution. Membrane fractions were prepared from one kidney, while the contralateral kidney was perfusion-fixed for immunocytochemistry. Immunoblotting and densitometry revealed a decrease in AQP2 levels to 27+/-3.4% of control levels (n=11, P<0.001) in inner medulla, and 34+/-15% of controls (n=5, P<0.05) in cortex. Urine production increased in parallel, from 11+/-1.4 to 30+/-4.4 ml/day (n=11, P<0.01). After return to a potassium-containing diet both urine output and AQP2 labels normalized within 7 d. Immunocytochemistry confirmed decreased AQP2 labeling in principal cells of both inner medullary and cortical collecting ducts. AQP2 labeling was predominantly associated with the apical plasma membrane and intracellular vesicles. Lithium treatment for 24 d caused a more extensive reduction of AQP2 levels, to 4+/-1% of control levels in the inner medulla and 4+/-2% in cortex, in association with severe polyuria. The similar degree of downregulation in medulla and cortex suggests that interstitial tonicity is not the major factor in the regulation of AQP2 expression. Consistent with this furosemide treatment did not alter AQP2 levels. In summary,hypokalemia, like lithium treatment, results in a decrease in AQP2 expression in rat collecting ducts, in parallel with the development of polyuria, and the degree of downregulation is consistent with the level of polyuria induced, supporting the view that there is a causative link.
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PMID:Hypokalemia-induced downregulation of aquaporin-2 water channel expression in rat kidney medulla and cortex. 862 81

1. Besides clinical use, there are many explanations for the mechanism of action of lithium. Although it is shown that lithium may reduce the supply of inositol that is required to sustain phosphoinositide synthesis, evidence exists concerning the potentiating effect of lithium on this pathway. We therefore decided to evaluate conditions in which lithium inhibits or potentiates platelet aggregation and calcium response induced by vasopressin. 2. Platelet aggregation was measured by the photometric method, and changes in intracellular free calcium were measured using fura-2/AM. 3. We show an inhibitory action of neomycin on vasopressin-induced platelet aggregation. Lithium, according to the preincubation time, could both potentiate or inhibit platelet aggregation and calcium responses induced by vasopressin. The inhibitory effect of lithium on platelet aggregation is dependent on concentrations of both lithium and vasopressin and also the presence of indomethacin, for example, in the absence of indomethacin there was no clear inhibitory action of lithium on vasopressin-induced platelet aggregation. 4. These results show the importance of arachidonate metabolites concerning lithium effects on platelet V1-receptor signaling. In conclusion, because the arachidonate metabolites are responsible for the release of other active substances from platelets' granules, the aggregatory responses in the absence of indomethacin may be amplified, and this subsequently may change the net inhibitory action of lithium.
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PMID:Conditions that lithium inhibits or potentiates vasopressin V1-receptor-mediated platelet aggregation and [Ca++]i mobilization. 874 53


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