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)

We have characterized a Na+-K+-Cl- cotransporter in vascular endothelial cells (EC) cultured from different blood vessels and species that is inhibited by the diuretics furosemide and bumetanide (50% inhibitory concentration for 86Rb influx approximately 20 microM and 0.5 microM, respectively). Inward 86Rb influx mediated via this pathway is greater than 86Rb influx transported by the Na+-K+ pump in cultured EC from bovine and pig aorta, bovine vena cava, and baboon cephalic vein but not in human umbilical or saphenous vein EC. External Na+ or Cl- -stimulated, ouabain-insensitive 86Rb influx is equal to furosemide or bumetanide-sensitive 86Rb influx. Ouabain-insensitive 22Na influx is also partially inhibited by these drugs and stimulated by increasing external K+ or Cl-. Net Na+ extrusion occurs via the Na+-K+-Cl- cotransporter in the absence of external K+, whereas net Na+ influx occurs at higher external K+ (greater than 1 mM). Maximal concentrations (100 nM) of bradykinin and vasopressin increase the initial rate of bumetanide-sensitive 86Rb influx by approximately 60 and 70% (50% effective concentration approximately 1 and 0.6 nM, respectively). Addition of either ethyleneglycol-bis(beta-aminotethylether)-N,N'-tetraacetic acid or LaCl3 (to block calcium influx) prevents bradykinin-stimulated 86Rb influx. When intracellular calcium is elevated using ionomycin (100 nM), a Ca2+ ionophore, bumetanide-sensitive 86Rb influx increases approximately twofold. In contrast, isoproterenol (100 microM) and forskolin (50 microM), adenylate cyclase stimulators, decrease furosemide-sensitive 86Rb influx.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Bradykinin and vasopressin stimulate Na+-K+-Cl- cotransport in cultured endothelial cells. 371 30

The mammalian antidiuretic hormone, 8-arginine-vasopressin, was found to increase net mucosal-to-serosal urea flux across the isolated toad urinary bladder 13-fold. This urea flux was accompanied by a 24-fold increase in solute-linked water movement across the membrane. Net urea flux and urea-linked volume flux were inhibited by 50% or more when thiourea was added to the mucosal medium at concentrations equal to those of urea. In contrast, thiourea did not inhibit osmotic water flux across the bladder in the presence of vasopressin. These observations are consistant with the view that thiourea and urea compete for a common site on a membrane carrier molecule. When bladders were exposed to vasopressin on the serosa and subsequently fixed with 1% glutaraldehyde on the mucosa, they were found to retain 74% of their prefixation permeability to urea. Net urea flux across these fixed bladders (in the absence of vasopressin) was markedly inhibited by thiourea, whereas osmotic water flux was not inhibited. These studies suggest that vasopressin induces the formation of "urea-channels" in the membrane that can be preserved by glutaraldehyde and blocked by thiourea.
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PMID:Inhibition of vasopressin-stimulated urea transport across the toad bladder by thiourea. 420 Dec 69

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

1. Net water flow J(w), was measured across the abdominal skin of the toad Bufo marinus with a volumetric, automatic technique that allows for averaging J(w) over time intervals as short as 1 sec.2. Basal J(w) was very stable and corresponded to a coefficient of osmotic flow, L(PD), of ca. 15 x 10(-7) cm sec(-1) atm(-1) (or to an osmotic water permeability coefficient, P(f), of 20 mum sec(-1)).3. Both vasopressin and the beta-adrenergic agonist, isoprenaline, triggered high hydrosmotic responses that could lead to P(f) values exceeding 250 mum sec(-1). The effect of isoprenaline was very reproducible while that of vasopressin varied considerably.4. Methohexital and propranolol selectively inhibited the hydrosmotic effects of vasopressin and isoprenaline, respectively, whereas amiloride and ouabain had no effect.5. Mutual inhibition was found between vasopressin and isoprenaline in skins very sensitive to vasopressin. In less sensitive skins isoprenaline further increased J(w) despite exposure of the epithelia to supramaximal concentrations of vasopressin.6. Differential reactivity to vasopressin was found between the skin and the bladder taken from the same toad. In some instances, the bladder responded normally to vasopressin while the skin was totally unresponsive, suggesting the presence of osmoregulatory mechanisms exerting a local modulation of the vasopressin action in different target epithelia of the same animal.
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PMID:Osmotic water flow across the abdominal skin of the toad bufo marinus: effect of vasopressin and isoprenaline. 681 22

Controls for glomerular filtration (GFR) and tubular transport of solutes and water are interrelated. GFR changes with hydration, apparently as a result of changes in the number of filtering nephrons under the control of antidiuretic hormone. The resulting alterations in volume flow rate through the collecting ducts may be as important as changes in epithelial permeability in determining urine osmolarity. Tubular transport of sodium and potassium may be controlled in part by antidiuretic hormone and aldosterone but considerable variation occurs among species, and intrinsic regulation of distal tubular sodium absorption in response to the delivered load of sodium may also occur. Net tubular secretion of phosphate, under control of parathyroid hormone, occurs in some species, but no hormonal control of tubular calcium transport has been demonstrated. Net tubular urate secretion that is influenced by potassium occurs in uricotelic reptiles. Complexing of inorganic cations, especially sodium and potassium, with urate precipitates in tubular urine permits excretion of cations without their contributing to urine osmolarity. This process also may keep the distal tubule sodium concentration low enough to permit maximum dilution but may require absorption of filtered water without sodium. Such an absorptive process may exist in reptilian proximal tubules.
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PMID:Reptilian glomerular and tubular functions and their control. 708 82

A study was made of the initial responses of perfusate Ca2+ fluxes and bile flow to Ca(2+)-mobilizing agonists, following refinements to the methods for analysing these parameters in the perfused rat liver. Net Ca2+ efflux induced by vasopressin commences at 15 s, reaches a maximal rate at 35 s and declines to zero by 55 s, when Ca2+ influx commences. Vasopressin-induced increases in bile flow commence by 20 s, attain a maximal rate by 35 s and begin to decline at 50 s, to reach basal values by 90 s. Concomitant administration of glucagon modifies each of these actions of vasopressin in the following ways: it decreases by 5 s the time of onset of net Ca2+ efflux, and the time and magnitude of such efflux, and the time of onset of bile flow is decreased to 15 s, and the flow reaches maximal rates by 30 s. When the alpha 1-adrenergic agonist phenylephrine is used in place of vasopressin, Ca2+ efflux commences at 17-18 s and is greater in magnitude; little bile flow is induced by this agonist. Glucagon modifies the action of phenylephrine in the following ways: the onset of Ca2+ efflux is brought forward by 2-3 s, it is of lower magnitude and Ca2+ influx begins by 45 s; bile flow commences by 15-20 s, and reaches a maximum at 30 s, where the rate is much greater than in the absence of glucagon; this rate gradually declines to be near basal by 80 s. The onset of agonist-induced oxygen uptake was also brought forward by the co-administration of glucagon. Comparison of agonist-induced plasma-membrane Ca2+ fluxes and bile flow (with or without glucagon administration) suggests that correlations can be made between net Ca2+ fluxes and the transient increases seen in bile flow.
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PMID:The synergistic action (cross-talk) of glucagon and vasopressin induces early bile flow and plasma-membrane calcium fluxes in the perfused rat liver. 803 69

We reported that feeding rats 8% protein for 4 wk induces two new urea transport processes in initial inner medullary collecting ducts (IMCD); neither is present in rats fed 18% protein. In this study, we measured the time course of induction of these transporters in perfused initial IMCD segments from rats fed 8% protein. Net urea flux was induced after 3 wk, whereas vasopressin-stimulated passive urea permeability (P(urea)) was induced after 2 wk. 8-Bromoadenosine 3',5'-cyclic monophosphate (8-BrcAMP) significantly increased P(urea)); adding vasopressin did not increase P(urea) further. In fact, there was no difference in vasopressin-stimulated cAMP production in initial or terminal IMCD segments from rats fed 18% or 8% protein, suggesting that the adaptive response was not due to increased cAMP production. Glucagon did not change cAMP production or P(urea). Specificity of the response was suggested because neither aldose reductase nor sorbitol dehydrogenase activity changed with feeding 8% protein. Thus 1) in initial IMCD segments, vasopressin-stimulated P(urea) is induced after 2 wk, but net urea flux requires 3 wk of feeding 8% protein; 2) this adaptation is not solely due to a higher rate of cAMP production; and 3) specificity of the adaptive response is suggested because activities of enzymes responding to decreases in concentrating ability are unchanged. These results suggest that two distinct urea transporters may be involved in the adaptation to a low-protein diet.
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PMID:Protein restriction sequentially induces new urea transport processes in rat initial IMCD. 820 59

Low protein diets reverse the urea concentration gradient in the renal inner medulla. To investigate the mechanism(s) for this change, we studied urea transport and cell ultrastructure in initial and terminal inner medullary collecting ducts (IMCD) from rats fed 18% protein or an isocaloric, 8% protein diet for 4 wk. Serum urea, aldosterone, and albumin were significantly lower in rats fed 8% protein, but total protein and potassium were unchanged. Vasopressin stimulated passive urea permeability (Purea) threefold (P < 0.05) in initial IMCDs from rats fed 8% protein, but not from rats fed 18% protein. Luminal phloretin reversibly inhibited vasopressin-stimulated Purea. However, in terminal IMCDs from rats fed either diet, vasopressin stimulated Purea. Net transepithelial urea flux (measured with identical perfusate and bath solutions) was found only in initial IMCDs from rats fed 8% protein. Reducing the temperature reversibly inhibited it, but phloretin did not. Electron microscopy of initial IMCD principal cells from rats fed 8% protein showed expanded Golgi bodies and prominent autophagic vacuoles, and morphometric analysis demonstrated a marked increase in the surface density and boundary length of the basolateral plasma membrane. These ultrastructural changes were not observed in the terminal IMCD. Thus, 8% dietary protein causes two new urea transport processes to appear in initial but not terminal IMCDs. This is the first demonstration that "active" urea transport can be induced in a mammalian collecting duct segment.
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PMID:Low protein diet alters urea transport and cell structure in rat initial inner medullary collecting duct. 822 60

1. Net water flow (Jw) was continuously monitored across the abdominal skin of the toad Bufo marinus by means of a volumetric, automatic technique. Jw was either averaged over periods of 2 min or taken cumulatively (10 or 30 min periods). 2. The state of high water permeability induced by vasopressin or isoprenaline was reversed (88-89% inhibition of delta Jw after 1 h) by the addition of 10(-3) M HgCl2 (or CH3ClHg) to the external bathing medium. Similarly, pre-exposure of the skins to Hg2+, totally blocked the induction of the hydrosmotic response to the same agents. By itself, Hg2+ exerted only a minor (26%) stimulation of basal Jw. 3. There was a sigmoidal dose-response relationship between the reduction of the hydrosmotic effect of vasopressin (VP) and the concentration of Hg2+ in the external medium, with a half-maximal effect at 1.2 x 10(-4) M HgCl2. 4. Total replacement of Na+ by K+, Rb+ or Cs+ in the Ringer solution, caused a VP-like, hydrosmotic effect that was reversed, or prevented, by exposure to Hg2+ in a manner indistinguishable from that previously seen with vasopressin or isoprenaline. 5. The data point to the presence of a Hg(2+)-sensitive apical water pathway in stimulated epithelia, very probably constituted by water channels similar to those reported in red blood cells, amphibian bladder and mammalian kidney tubules.
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PMID:Mercury blockage of apical water channels in toad skin (Bufo marinus). 825 34

Active reabsorption of urea appears in the initial IMCD (IMCD1) of rats fed a low-protein diet. To determine whether active urea transport also occurs in the deepest IMCD subsegment, the IMCD3, we isolated IMCDs from the base (IMCD1), middle (IMCD2), and tip (IMCD3) regions of the inner medulla from rats fed a normal protein diet and water ad libitum. IMCDs were perfused with identical perfusate and bath solutions. A significant rate of net urea secretion was present only in IMCD3s. Replacing perfusate Na+ with NMDG+ reversibly inhibited net urea secretion but replacing bath Na+ with NMDG+ or perfusate Cl- with gluconate- had no effect. Net urea secretion was significantly inhibited by: (a) 250 microM phloretin (perfusate); (b) 100 nM triamterene (perfusate); (c) 1 mM ouabain (bath); and (d) cooling the tubule to 23 degrees C. Net urea secretion was significantly stimulated by 10 nM vasopressin (bath). Next, we perfused IMCD3s from water diuretic rats (given food ad libitum) and found a significant, fivefold increase in net urea secretion. In summary, we identified a secondary active, secretory urea transport process in IMCD3s of normal rats which is upregulated in water diuretic rats. This new urea transporter may be a sodium- urea antiporter.
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PMID:Evidence for sodium-dependent active urea secretion in the deepest subsegment of the rat inner medullary collecting duct. 943 15


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