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)

Urea transport across the terminal inner medullary collecting duct (IMCD) is mediated by a urea transporter that is stimulated by vasopressin (AVP) or hyperosmolarity. To determine whether hyperosmolarity stimulates urea transport by an adenylyl cyclase-dependent or -independent mechanism, terminal IMCDs were perfused with 10 microM forskolin followed by an increase in osmolality or with increasing osmolality followed by 10 nM AVP. In both protocols, stimulating adenylyl cyclase caused an additive increase in urea permeability (Purea) to that stimulated by hyperosmolarity. Next, we investigated whether hyperosmolarity stimulates the same urea transporter as AVP by studying the inhibitor profile and IMCD subsegment response of hyperosmolarity-stimulated urea transport and comparing it to properties already demonstrated for AVP-stimulated urea transport. In terminal IMCDs, luminal phloretin (250 microM) reversibly inhibited Purea by 63%. Thiourea (100 mM) inhibited Purea by 73% at two different levels of osmolality, 690 and 290 mosmol/kgH2O. The half-maximal inhibitory concentration (K1/2) for thiourea at 690 mosmol/kgH2O was not significantly different from the K1/2 value at 290 mosmol/kgH2O, suggesting that stimulation by hyperosmolarity is related to an increase in the Vmax for the urea transporter. Finally, we found that hyperosmolarity did not stimulate Purea in the initial IMCD. In summary, the data suggests that hyperosmolarity stimulates urea transport by an adenylyl cyclase-independent mechanism. However, the inhibitor profile and the IMCD subsegment response for hyperosmolarity-stimulated and AVP-stimulated Purea are similar, suggesting that both hyperosmolarity and AVP stimulate the same urea transporter.
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PMID:Characteristics of osmolarity-stimulated urea transport in rat IMCD. 162 10

The vasopressin-dependent urea permeability of the rat terminal inner medullary collecting duct (IMCD) is much greater than can be explained by lipid-phase permeation or paracellular diffusion, suggesting the presence of vasopressin-stimulated facilitated transport pathway. We used the isolated perfused tubule technique to test whether the urea transport pathway exhibits saturation characteristics consistent with a facilitated pathway. When the luminal urea concentration was varied between 0 and 800 mM (no urea in peritubular bath), the relationship between the urea flux and the luminal concentration was linear with a y-axis intercept that was not significantly different from zero, indicating an absence of saturation in this concentration range. Higher concentrations of urea could not be tested due to technical limitations. However, when thiourea (a urea analogue that shares the urea transport pathway with urea) was substituted for urea in similar experiments, the apparent thiourea permeability fell with increasing thiourea concentration in the range 10-200 mM, indicative of saturation of the urea-thiourea transporter. When the urea concentration was varied in both bath and lumen, the lumen-to-bath urea flux approached a limiting value at 400-500 mM urea, consistent with saturation of the transporter. However, nonspecific inhibition of urea transport by bath urea could not be ruled out in those experiments. We conclude that the urea and thiourea transport pathway in the terminal IMCD exhibits saturation characteristics. However, the urea concentration required to saturate the pathway is apparently high, at least 400-500 mM in one set of experiments and probably greater than 800 mM in another.
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PMID:Concentration dependence of urea and thiourea transport in rat inner medullary collecting duct. 210 58

Isoprenaline, a beta adrenergic agonist, strongly increases both transepithelial fluxes across the urinary bladder of Bufo bufo; this effect is dose dependent, 10(-6)M being necessary for the maximal action. This effect is less selective than that of vasopressin: the ratio J urea/J thiourea is 3.8 under isoprenaline and 30.4 under vasopressin treatment. Both hormones differently affect the permeability of a mainly liposoluble molecule, i.e. antipyrine: vasopressin increases antipyrine permeability, while isoprenaline decreases it. Moreover diethylpyrocarbonate treatment of the luminal membrane strongly inhibits vasopressin effect on urea permeability leaving unmodified that of isoprenaline. However, the actions of both hormones are not additive. These results allows to assume that the tissue has a feedback mechanism which inhibits other hormonal action while the bladder is stimulated by a particular hormone.
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PMID:Permeability properties of the Bufo bufo bladder as affected by isoprenaline and vasopressin. 248 13

Arginine vasopressin (AVP) increases the urea permeability of the rat terminal inner medullary collecting duct (IMCD) to levels much greater than can be explained by lipid-phase permeation or paracellular diffusion, suggesting the presence of an AVP-stimulated facilitated transport pathway. We tested whether inhibitors of facilitated urea transport in erythrocytes and toad bladder also inhibit urea transport in the isolated perfused IMCD. Apparent urea permeability (Purea) was determined by measuring the flux due to an imposed 5 mM concentration gradient. Phloretin (0.25 mM in lumen or bath) reversibly inhibited Purea. Phloretin, however, did not alter the osmotic water permeability. Urea analogues (200 mM) in the bath inhibited Purea (thiourea, 74% inhibition; methylurea 65%; acetamide 35%). Urea analogues in the lumen decreased Purea with the same order of potency. The inhibitory K1/2 for thiourea in the lumen was 27 +/- 2 mM and did not change with 10(-10) M AVP (28 +/- 3), despite a fourfold increase in Purea. We conclude the following. 1) Inhibitor actions on urea transport in the IMCD are similar to those in red blood cells and toad bladder, suggesting that the urea transporter could be a membrane protein similar to that in the other tissues. 2) Inhibition of Purea by phloretin without an effect on vasopressin-stimulated water permeability supports the view that the urea pathway is not the vasopressin-stimulated water channel. 3) The ability of AVP to increase Purea without an effect on the inhibitory K1/2 for thiourea indicates that AVP probably does not act by altering the binding affinity of individual transporters for urea.
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PMID:Inhibition of urea transport in inner medullary collecting duct by phloretin and urea analogues. 250 65

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

It is generally believed that urea crosses the cell membrane through aqueous channels, and that its movement across the membrane is accelerated in the direction of net water flow (solvent drag effect). The present report presents evidence for a vasopressin-sensitive pathway for the movement of urea, other amides, and certain non-amides, which is independent of water flow. Phloretin, when present at 10(-4) M concentration in the medium bathing the luminal surface of the toad bladder, strongly inhibits the movement of urea, acetamide, and propionamide across the toad bladder, both in the absence and presence of vasopressin. The vasopressin-stimulated movement of formaldehyde and thiourea is also reduced. Osmotic water flow, on the other hand, is not affected; nor is the movement of ethanol and ethylene glycol, or the net transport of sodium. On the basis of these studies we would conclude that the movement of many, if not all, solutes across the cell membrane is independent of water flow, and that a vasopressin-sensitive carrier may be involved in the transport of certain solutes across the cell membrane.
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PMID:Effect of phloretin on water and solute movement in the toad bladder. 470 29

The isotopic equilibration of urea, thiourea, and inulin between urine and plasma was determined in rabbits in the presence or absence of antidiuretic hormone (ADH). Animals were anesthetized with ethanol and permitted to reach steady state after completion of surgery. Tracer was then administered by intraarterial infusion in such a manner that a high constant specific activity in plasma was rapidly attained. Urine flow was kept independent of ADH by addition of mannitol. Urea/creatinine clearance ratios and the accumulation of urea in renal medulla and papilla also remained unaffected by ADH. Under these conditions, thiourea and inulin at all times approached equilibrium, at similar rates. In the absence of ADH, urea also equilibrated at a rate similar to that of inulin. The addition of ADH, however, significantly prolonged the delay before urinary urea reached the high constant specific activity of plasma urea. These observations are interpreted in terms of a specific effect of the hormone on the solute permeability of the nephron.
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PMID:The action of pitressin on solute permeability of the rabbit nephron in vivo. 597 Oct 28

The addition of the Ca++ ionophore A23187 (10 microM) to the inside solution of the frog skin induced a transient increase in the active Na+ transport in frog skin (Rana esculenta) which decayed to the control values 60 minutes after the addition. At the same time the skin resistance failed significantly; antidiuretic hormone addition resulted in no-more increase of the Na+ active transport; the skin resistance remained unchanged. To further investigate the role of intracellular calcium on the skin transepithelial permeability, the effect of A23187 ionophore on thiourea permeability has been tested. Increase in intracellular Ca++ concentration brought about by calcium ionophores have been shown to modify both basal and ADH-stimulated thiourea transport.
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PMID:[Effect of ionophore A23187 on the response to ADH in the ventral skin of Rana esculenta]. 641 90

We have employed a variety of urea and thiourea analogues to elucidate further the vasopressin-stimulated urea transport mechanism. In the urea series there was a progressive inhibition of tracer urea transport as cylindrical radius of analogue increased from 2.9 to 3.5 A. Above 3.8 A no inhibition was found. Thiourea analogues were more potent inhibitors for comparable cylindrical radii, and compounds greater than 3.8 A again were not inhibitory. Inhibition was comparable when the inhibitor was moving in the same or opposite directions. Urea transport and its inhibition were preserved in bladders fixed with glutaraldehyde. Osmotic water flow, tritiated water flow, and uric acid transport were not affected by any analogues tested. Analogues of urea and thiourea affected the transport of labeled methylurea and thiourea in a manner similar to their effect on urea. We therefore propose that the urea transport mechanism is a channel with a cylindrical radius between 3.5 and 3.8 A that is capable of interaction with the moving species by hydrogen bonding. This model can account for the selectivity of the vasopressin-stimulated urea transport, its inhibition by urea and thiourea analogues, the facilitated transport of urea, inhibition of tracer urea flux from either the cis or the trans position, and finally the preservation of the urea transport machinery following glutaraldehyde fixation.
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PMID:Importance of molecular size and hydrogen bonding in vasopressin-stimulated urea transport. 680 2

Acetohydroxamic acid (AHA), a urea analogue, is used clinically to dissolve struvite stones because it inhibits the urease produced by Proteus mirabilis. To be effective, the concentration of AHA must be high in the collecting duct system and final urine. Because AHA is structurally similar to urea, we investigated whether AHA is transported by the urea carrier found in the terminal inner medullary collecting duct (IMCD) and the erythrocyte. We examined AHA transport under four conditions known to affect urea movement across the terminal IMCD, i.e., stimulation by vasopressin (AVP) and hyperosmolality, and inhibition by phloretin and urea analogues. The AHA permeability was determined with a 10 mM bath-to-lumen AHA gradient. AHA was measured by ultramicrocolorimetry. Addition of 1 nM AVP to the bath increased the AHA permeability of the perfused terminal IMCD. Increasing perfusate and bath osmolality from 290 to 690 mosmol/kgH2O (by adding NaCl) also increased tubule permeability to AHA. Addition of either 0.25 mM phloretin to the bath or 200 mM thiourea to the lumen reversibly inhibited the AVP-stimulated AHA permeability. AHA-induced osmotic lysis of erythrocytes was inhibited by phloretin or thionicotinamide; AHA inhibited the osmotic lysis induced by the urea analogue acetamide. Thus, in the rat terminal IMCD, both urea and AHA transport are stimulated by AVP and hyperosmolality, and both are inhibited by phloretin and thiourea. In erythrocytes, both urea and AHA transport are inhibited by phloretin or thionicotinamide. Thus AHA is transported by the urea carrier in the terminal IMCD and erythrocyte.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The urease inhibitor acetohydroxamic acid is transported by the urea pathway in rat terminal IMCD. 821 97


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