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 effects of prostaglandin synthesis inhibition by naproxen were studied in toad bladder. Luminal membrane water permeability was evaluated both by the frequency of intramembranous particle aggregates in granular cell luminal membrane and by direct assessment of the rate of change of cell volume during perfusion of an anisosmotic solution. Total tissue water permeability was assessed by transbladder osmotic water flow. Inhibition of prostaglandin synthesis caused luminal membrane water permeability to increase much more than expected from tissue permeability measurements. The addition of a very low dose of antidiuretic hormone (ADH) (0.125 mU/ml) during prostaglandin synthesis inhibition increased luminal membrane water permeability to the same level as maximal stimulation with ADH, while tissue water permeability failed to increase proportionately. The results imply the presence of a regulatable barrier to water movement across toad bladder that is distal to the luminal membrane and subject to control by either prostaglandins or ADH.
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PMID:Regulation of water permeability in toad urinary bladder at two barriers. 391 61

The effect of vanadate, a potent inhibitor of Na-K-ATPase, on the hydroosmotic response to vasopressin (AVP) and transepithelial voltage (Vt) in cortical collecting tubules was examined. At 37 degrees C, exposure of collecting tubules to bath vanadate (10(-4) M) for 30 min inhibited the increase in hydraulic water permeability (Lp) in response to AVP or 8-bromo-cyclic adenosine monophosphate by 68 and 76%, respectively. When vanadate was present only in the lumen no inhibition of the AVP response was observed. Incubation of tubules with ouabain (10(-5) M) for 30 min inhibited the AVP-induced increase in Lp to the same extent as vanadate. At 25 degrees C, vanadate inhibited the increase in Lp by AVP if added before but not after the hormone. Addition of vanadate to the bath caused a rapid decrease in the lumen-negative Vt that is consistent with Na-K-ATPase inhibition. Luminal vanadate also inhibited Vt but the rate of decrease of Vt was much slower than in the presence of bath vanadate. We conclude that vanadate inhibits the development but not the maintenance of the AVP-induced increase in water permeability in the collecting tubule. Since the effect of ouabain was similar to that of vanadate, the results suggest that inhibition of Na-K-ATPase directly or indirectly interferes with the initiation of the AVP-induced increase in luminal membrane water permeability at a site distal to cAMP formation.
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PMID:Inhibition of vasopressin action by vanadate in the cortical collecting tubule. 655 36

We investigated immunohistochemical localization of V2 vasopressin receptor along the nephron using a specific polyclonal antibody. Staining was observed in some of thick ascending limbs and all of principal and inner medullary collecting duct (IMCD) cells. Not only basolateral but also luminal membrane was stained in collecting ducts, especially in terminal IMCD (tIMCD). To learn the functional role of luminal V2 receptor in tIMCD, we studied the luminal effects of arginine vasopressin (AVP) on osmotic water permeability (Pf), urea permeability (Pu), and cAMP accumulation using isolated perfused rat tIMCD. In the absence of bath AVP, luminal AVP caused a small increase in cAMP accumulation, Pf and Pu, confirming the presence of V2 receptor in the lumen of tIMCD. In contrast, luminal AVP inhibited Pf and Pu by 30-65% in the presence of bath AVP by decreasing cAMP accumulation via V1a or oxytocin receptors and by an unknown mechanism via V2 receptors in the luminal membrane of tIMCD. These data show that V2 receptors are localized not only in the basolateral membrane but also in the luminal membrane of the distal nephron. Luminal AVP acts as a negative feedback system upon the basolateral action of AVP in tIMCD.
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PMID:Immunohistochemical localization of V2 vasopressin receptor along the nephron and functional role of luminal V2 receptor in terminal inner medullary collecting ducts. 756 68

Secretion of bicarbonate has been described for distal nephron epithelium and attributed to apical Cl-/HCO3- exchange in beta-intercalated cells. We investigated the presence of this mechanism in cortical distal tubules by perfusing these segments with acid (pH 6) 10 mM phosphate Ringer. The kinetics of luminal alkalinization was studied in stationary microperfusion experiments by double-barreled pH (ion-exchange resin)/1 M KCl reference microelectrodes. Luminal alkalinization may be due to influx (into the lumen) of HCO3- or OH-, or efflux of H+. The magnitude of the Cl-/HCO3- exchange component was measured by perfusing the lumen with solutions with or without chloride, which was substituted by gluconate. This component was not different from zero in control and alkalotic (chronic plus acute) Wistar rats. Homozygous Brattleboro rats (BRB), genetically devoid of antidiuretic hormone, were used since this hormone has been shown to stimulate H+ secretion, which could mask bicarbonate secretion. In these rats, no evidence for Cl-/HCO3- exchange was found in control BRB and in early distal segments of alkalotic animals, but in late distal tubule a significant component of 0.14 +/- 0.033 nmol/cm2.sec was observed, which, however, is small when compared to the reabsorptive flow found in control Wistar rats, of 0.95 +/- 0.10 nmol/cm2.sec. In addition, 5 x 10(-4) M SITS had no effect on distal bicarbonate reabsorption in controls as well as on secretion in alkalotic Wistar and Brattleboro rats, which is compatible with the absence of effect of this drug on the apical Cl-/HCO3- exchange in other tissues.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Secretion of HCO3-/OH- in cortical distal tubule of the rat. 776 8

Although vasopressin V1 receptors have been shown to exist in both luminal and basolateral membranes of rabbit cortical collecting duct (CCD), exact cell types having V1 receptors remain unestablished. To identify the distribution of V1 receptor by cytoplasmic Ca2+ response, we utilized the confocal imaging system in the microperfused rabbit CCD. Basolateral application of arginine vasopressin (AVP) increased [Ca2+]i mainly in one group of cells which were not stained by fluorescein-isothiocyanate-conjugated peanut agglutinin. Luminal application of AVP increased [Ca2+]i in the same cells which responded to basolateral AVP. These findings provide evidence that V1 receptors, as defined by the [Ca2+]i response, exist in both luminal and basolateral membranes of the rabbit principal cell.
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PMID:Cell Ca2+ response to luminal vasopressin in cortical collecting tubule principal cells. 819 83

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

The aim of the present study was to determine whether vasopressin affects NaCl reabsorption in the medullary thick ascending limb of the loop of Henle when administered selectively to the luminal membrane. At 5 x 10(-6) M and 10(-8) M, luminal [Arg8]vasopressin significantly inhibited Cl- transport in the in vitro microperfused rat medullary thick ascending limb by 46.4 +/- 5.9% (P < 0.01) and 32.4 +/- 2.0% (P < 0.05) respectively. The response to 10(-8) M luminal [Arg8]vasopressin was completely blocked by the vasopressin V1 receptor antagonist [beta-mercapto-beta,beta-cyclopenta-methylenepropionyl1, O-Me-Tyr2,Arg8]vasopressin (10(-6) M), and was mimicked by the vasopressin V1 receptor agonist [Phe1, Ile5, Orn8]vasopressin (10(-8) M; delta -35.0 +/- 4.5%; P < 0.05). Luminal administration of the vasopressin V2 receptor agonist [deamino-Cys1, D-Arg8]vasopressin (5 x 10(-6) M) had no effect on transport. These data suggest that luminal vasopressin can inhibit NaCl transport in the medullary thick ascending limb of the rat via vasopressin V1 receptors.
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PMID:Effect of luminal vasopressin on NaCl transport in the medullary thick ascending limb of the rat. 890 37

The aim of the study was to determine if and by what mechanism(s) nitric oxide inhibition modulates the susceptibility of the duodenum to hydrochloric acid-induced disturbances of mucosal integrity. A second aim was to investigate whether basal permeability is a determinant of epithelial acid barrier function. Using an in situ duodenal perfusion model, mucosal permeability, alkaline secretion and morphology were investigated in anaesthetized rats. Luminal perfusion with 50 mM hydrochloric acid increased duodenal mucosal permeability in the control animals. In animals receiving the nitric oxide synthase inhibitor N-nitro-L-arginine methyl ester (L-NAME 3 mg kg(-1) and 1 mg kg(-1) h(-1)) and in those receiving vasopressin (1 IU kg(-1) h(-1)), however, the mean increase in permeability in response to acid was markedly higher. In rats treated with either hexamethonium (20 mg kg(-1)) or atropine (0.5 mg kg(-1)) L-NAME failed to augment the acid-induced increase in permeability. Perfusion with hypotonic saline (25 mM) increased basal permeability but did not influence the response to acid. Exposure of the duodenum to hydrochloric acid caused very subtle changes of duodenal morphology. It is concluded that both inhibition of endogenous nitric oxide synthesis and vasopressin treatment augment the acid-induced increase in mucosal permeability. The mechanisms involved may be related to changes of Starling forces in the microcirculatory bed. Endogenous nitric oxide may protect the duodenal mucosa by regulating vascular permeability and interstitial fluid pressure.
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PMID:Acid-induced increase in duodenal mucosal permeability is augmented by nitric oxide inhibition and vasopressin. 933 17

Luminal perfusion with collected proximal fluid increases distal K(+) secretion compared with artificial solutions. Arginine vasopressin (AVP), present in luminal fluid, might be responsible for this observation. K(+) secretion rate (J(K)) was measured by K(+)-sensitive microelectrodes during paired luminal stationary microperfusion with control and AVP-containing 0.5 mM K(+) solutions. J(K) was 1.34 +/- 0.35 (n = 24 tubules) nmol x cm(-2) x s(-1) during perfusion with 10(-9) M AVP, against 0.90+/-0.12 nmol x cm(-2) x s(-1) (n = 21) in control (P<0.02). With 10(-9) M AVP+10(-6) M beta-mercapto-beta-beta-cyclopenta-methylenepropionyl(1), O-Me-Tyr(2)-Arg(8) vasopressin (MCMV), a specific peptide V(1)-receptor antagonist, J(K) was 0.36+/-0.067 against 0.77+/-0.10 (control; n = 9) nmol x cm(-2) x s(-1) (P<0.01). With 10(-6) M MCMV alone, J(K) was 0.37+/-0.04 against a control of 0.62+/-0.06 (n = 19) nmol. cm(-2). s(-1) (P<0.01). A peptide V(2) antagonist had no such effect. In Brattleboro rats, which do not produce endogenous AVP, MCMV had no effect when given alone, although AVP still stimulated J(K). In conclusion, luminal AVP stimulates distal J(K) significantly. The V(1) antagonist MCMV inhibits the effect of AVP but also reduces J(K) when given alone. This suggests that AVP acts luminally via V(1) receptors but also that there appears to be a background effect of endogenous AVP blocked by the antagonist.
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PMID:V(1) receptors in luminal action of vasopressin on distal K(+) secretion. 1080 93