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)

Turtle urinary bladder possesses four ion transport processes: Na+ absorption, H+ secretion, and HCO3- secretion-Cl- absorption. Each transport process is performed by a specific epithelial cell type. Granular cells absorb Na+ but they are not sensitive to antidiuretic hormone (ADH), unlike toad bladder granular cells. alpha-Carbonic anhydrase-rich (CA) cells secrete H+ via an apical H+-adenosinetriphosphatase (ATPase). Under conditions of low CO2 tension, this active pump is contained in the limiting membranes of certain cytoplasmic vesicles. The vesicles fuse with the apical membrane, and H+ pumps are incorporated into that membrane, as physiological conditions demand increased H+ secretion. The stimulus for fusion of these vesicles with the apical membrane appears to be intracellular acidification. beta-CA cells secrete HCO3- and reabsorb Cl-, both processes driven by H+-ATPase in the basolateral membrane in series with an apical Cl- -HCO3- exchanger. Increased intracellular adenosine 3',5'-cyclic monophosphate concentration in beta-cells stimulates net HCO3- secretion and induces an electrogenic component of this flux by activating an apical Cl- channel. This activation accompanies the fusion of an intracellular tubulovesicular network with the apical membrane. The membrane of this network may contain Cl- channels.
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PMID:Turtle urinary bladder: regulation of ion transport by dynamic changes in plasma membrane area. 251 70

We assembled a new system using a lucite chamber and rat stomach for simultaneous measurement of transmucosal potential difference (PD) and luminal pH as indicators of the mucosal integrity and the secretory activity, respectively. The biological preparation involved only the glandular mucosa and responded to a variety of mucosal damaging agents by different degrees of PD reduction, pH increases and histological damages. When the mucosa was exposed for 10 min to 1 M NaCl, the reduced PD was restored with time, reaching the baseline values within 2 hr with histological restitution. Titration of gastric effluent showed that after the exposure, acid secretion ceased and a considerable amount of HCO3- was evident in the lumen, followed by re-secretion of acid. These secretory changes corresponded with those of luminal pH; this remained elevated for 1 hr after the exposure and returned to the basal values 2 hr later. The histological restitution as well as the PD recovery after damage were significantly interfered with by indomethacin (5 mg/kg, s.c.) or vasopressin (10 unit/kg/hr, i.v.), respectively, at the dose which inhibited the increased pH responses caused by 1 M NaCl or reduced the mucosal blood flow. These results suggest that this system may be useful for studying physiological changes of gastric mucosa after acute injury and for screening drugs that may have an effect on the repair process.
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PMID:A continuous monitoring of mucosal integrity and secretory activity in rat stomach: a preparation using a lucite chamber. 273 61

Single skins were analyzed by 31P-nuclear magnetic resonance (NMR) spectroscopy during alternate perfusion with control and experimental solutions. Intracellular (pHc) and extracellular (pHo) pH were monitored by measuring the spectral frequencies of intracellular Pi and external methylphosphonate, respectively. Base-line pHc was 7.20 +/- 0.02 (SE) when pHo was 6.99 +/- 0.02. A 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonic acid (SITS)-inhibitable, HCO3--dependent alkaline shift in pHc can be elicited by replacing external Cl- by gluconate or sulfate. We now report that this effect is observed even in sodium-free media. The substitution of gluconate for external Cl- has also been reported to shrink cell volume. This shrinkage can be minimized by replacing Cl- with gluconate during perfusion with hypotonic, rather than isotonic, media. Conducted in this manner, the anionic substitution produces a much smaller alkaline shift in pHc. Replacement of external NaCl with N-methyl-D-glucamine chloride acidified the cells reversibly by 0.22 +/- 0.02. In the presence of the Na-H antiport blocker 5-(N-methyl-N-isobutyl)amiloride (MIA), restoration of external Na+ did not increase pHc. Separate addition of MIA acidified the cells by 0.18 +/- 0.03. Adenosine 3',5'-cyclic monophosphate (cAMP) also alters pHc. Addition of 1 mM 8(4-chlorophenylthio)cAMP or 100 mU/ml vasopressin acidified the cells by 0.22 +/- 0.03 and by 0.14 +/- 0.04, respectively. The data suggest that frog skin regulates pHc by the parallel operation of Na-H and Na+-independent Cl-HCO3 antiports. Cell volume and cAMP may play regulating roles in this epithelium.
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PMID:Intracellular pH in frog skin: effects of Na+, volume, and cAMP. 283 87

Two mechanisms are involved in the regulation of the intracellular pH (pHi) of aortic smooth muscle cells: the Na+/H+ antiporter and a Na+-independent HCO3-/Cl- antiporter. The Na+/H+ antiporter acts as a cell alkalinizing mechanism. It is activated by vasopressin and by phorbol esters when cells are incubated in the presence of bicarbonate but is not affected in the absence of bicarbonate. The HCO3-/Cl- antiporter acts as a cell acidifying mechanism. Agents such as forskolin, 8-Br-cAMP, and isoproterenol which raise intracellular cAMP levels inhibit the HCO3-/Cl- antiporter by shifting its pHi dependence in the alkaline direction. Thus, within the same cell type, different hormones control pHi variations by acting on different pHi regulating systems. An increase in pHi can be achieved either by a stimulation of a cell alkalinizing mechanism or by inhibition of a cell acidifying mechanism. A change of the activity of one pHi regulating mechanism modifies the responsiveness of the other to regulatory agents. Bicarbonate turns on the HCO3-/Cl- antiporter, decreases pHi and allows its regulation by protein kinase C through the Na+/H+ antiporter. Inhibition of the HCO3-/Cl- antiporter by cAMP increases the pHi and switches off the protein kinase C-mediated regulation.
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PMID:Dual control of the intracellular pH in aortic smooth muscle cells by a cAMP-sensitive HCO3-/Cl- antiporter and a protein kinase C-sensitive Na+/H+ antiporter. 284 21

We studied the effects of cyclic AMP (cAMP) on HCO-3 transport by rabbit cortical collecting tubules perfused in vitro. Net HCO-3 secretion was observed in tubules from NaHCO3- loaded rabbits. 8-Bromo-cAMP-stimulated net HCO-3 secretion, whereas secretion fell with time in control tubules. Both isoproterenol and vasopressin (ADH) are known to stimulate adenylate cyclase in this epithelium; however, only isoproterenol stimulated net HCO-3 secretion. The mechanism of cAMP-stimulated HCO-3 secretion was examined. If both HCO-3 and H+ secretion were to occur simultaneously in tubules exhibiting net HCO-3 secretion, cAMP might increase the net HCO-3 secretory rate by inhibiting H+ secretion, by stimulating HCO-3 secretion, or both. These possibilities were examined using basolateral addition of the disulfonic stilbene (4,4'-diisothiocyanostilbene-2,2'-disulfonate (DIDS). In acidifying tubules from NH4Cl-loaded rabbits, DIDS eliminated HCO-3 reabsorption, a result consistent with known effects of DIDS as an inhibitor of H+ secretion. In contrast, cAMP left acidification (H+ secretion) intact. DIDS applied to HCO-3 secretory tubules failed to increase the HCO-3 secretory rate, indicating minimal H+ secretion in HCO-3 secreting tubules. Thus, inhibition of H+ secretion by cAMP could not account for the cAMP-induced stimulation of net HCO-3 secretion. cAMP-stimulated HCO-3 secretion was reversibly eliminated by 0 Cl perfusate, whereas luminal DIDS had no effect. Bath amiloride (1 mM) failed to eliminate cAMP-stimulated HCO-3 secretion when bath [Na+] was 145 mM or 5 mM. cAMP depolarized the transepithelial voltage. The collected fluid [HCO-3] after cAMP could be accounted for by electrical driving forces, suggesting that cAMP stimulates passive HCO-3 secretion. However, cAMP did not alter HCO-3 permeability measured under conditions expected to inhibit transcellular HCO-3 movement (0 Cl- solutions and bath DIDS). This measured HCO-3 permeability was not high enough to account, by passive diffusion, for the HCO-3 fluxes observed in Cl-containing solutions. We conclude the following: cAMP increased net HCO3- secretion by stimulating HCO3- secretion and not by inhibiting H+ secretion; this HCO3- secretion may have occurred by Cl-HCO3- exchange; Na+-H+ exchange appeared not to play a role in basolateral H+ extrusion under these conditions; and the stimulation of HCO3- secretion by isoproterenol, but not ADH, suggests the existence of separate cell cAMP pools or cellular heterogeneity in this cAMP response.
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PMID:Cyclic adenosine monophosphate-stimulated bicarbonate secretion in rabbit cortical collecting tubules. 298 40

Differential interference contrast microscopy was used in combination with standard electrophysiological techniques in the in vitro perfused mouse medullary (mTALH) and cortical (cTALH) thick ascending limbs of Henle to evaluate the cell volume responses of these nephron segments to sudden increases in peritubular osmolality and to assess the role of antidiuretic hormone (ADH) and net NaCl absorption on hypertonic volume regulation. In the absence of CO2/HCO3- in external media, the cells of the mTALH behaved in a simple osmometric fashion, with an osmotic space equivalent to 70-80% of the total cell volume. However, in CO2/HCO3- -containing media, the cells of the mTALH, but not the cTALH, were able to increase their cell volume to the original volume after shrinkage in peritubular media made hypertonic with either NaCl or mannitol. This volume-regulatory increase response (VRI) in the mTALH was mediated by an increase in intracellular osmoles, and required peritubular ADH, at concentrations that stimulate maximally the rate of net NaCl absorption. This ADH effect on VRI could be mimicked by addition of dibutyryladenosine 3',5'-cyclic monophosphate to the bath in the absence of hormone. However, 10(-4) M luminal furosemide, a concentration that abolishes ADH-dependent NaCl absorption in the mTALH, had no effect on the VRI response. These results indicate that the cells of the mTALH, but not the cTALH, are capable of hypertonic volume regulation, that ADH (via adenosine 3',5'-cyclic monophosphate) is required for expression of the VRI response in the mTALH, and that the effects of ADH on net NaCl absorption and the VRI response in the mTALH are completely dissociable. Thus these results are consistent with a role for ADH in hypertonic VRI in the mammalian mTALH, which may operate to maintain constant cell volume in this nephron segment during antidiuresis.
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PMID:Hypertonic cell volume regulation in mouse thick limbs. I. ADH dependency and nephron heterogeneity. 301 18

Differential interference contrast microscopy and standard electrophysiological techniques were used to evaluate the transport processes involved in antidiuretic hormone (ADH)-dependent hypertonic cell volume regulation in the in vitro perfused mouse medullary thick ascending limb of Henle. Hypertonic cell volume regulation appeared to involve NaCl uptake into cells, since the cell volume increase after osmotic shrinkage in hypertonic media could be abolished either by symmetrical removal of Na+ from external solutions or by bath Cl- omission. The volume-regulatory process also required CO2/HCO3- in external media and could be abolished by the lipophilic carbonic anhydrase inhibitor, ethoxzolamide, in the presence of CO2/HCO3-. In addition, ADH-dependent hypertonic cell volume regulation was reduced or abolished by 10(-4) M amiloride, 10(-3) M ouabain, or 10(-4) M 4-acetamido-4'-isothiocyanostilbene-2,2-disulfonic acid in peritubular media or by cooling to 15 degrees C. In contrast, lumen Cl- omission or 10(-4) M amiloride addition to the perfusate had no effect on cell volume regulation in hypertonic peritubular media. These data suggest that ADH-dependent, hypertonic cell volume regulation in the mouse medullary thick limb depends on cell NaCl uptake via a secondary active transport process involving parallel Na+-H+ and Cl(-)-HCO3- exchangers in basolateral cell membranes. Finally, luminal furosemide (10(-4) M) abolished bath ouabain-mediated, rapid cell swelling in isotonic media containing ADH. Thus these exchangers do not appear to be active in the resting, isotonic state. The specific role of ADH in this NaCl transport process remains to be defined.
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PMID:Hypertonic cell volume regulation in mouse thick limbs. II. Na+-H+ and Cl(-)-HCO3- exchange in basolateral membranes. 301 19

The hormonal control of Cl transport was examined in rabbit cortical collecting tubules using the lumen-to-bath 36Cl tracer rate coefficient (KCl, nm/s). Tracer movement via Cl-HCO3 exchange was minimized by using HCO3-CO2-free solutions. The electrical driving force was minimized by treating with amiloride. Under these conditions, net Cl transport was zero, yet there was a large KCl that fell 88% on removing bath (trans) Cl. These results are consistent with the mechanism of tracer flux being predominantly Cl self exchange. KCl fell spontaneously with time in vitro; after this decline KCl could be stimulated with 8-bromo-cAMP. cAMP present from the onset of perfusion prevented the time-dependent fall in KCl. When tracer movement was restricted to diffusion by eliminating Cl self exchange (0 Cl bath), cAMP had no effect on KCl. Although both isoproterenol and vasopressin are known to stimulate adenylate cyclase in this epithelium, only isoproterenol mimicked the cAMP effect on KCl. The isoproterenol effect was blocked by either propranolol or prostaglandin E2. Lumen addition of the disulfonic stilbene DIDS had no effect on KCl. Lumen addition of furosemide or trichloromethiazide had minimal or no effect. Taken together, these results indicate that Cl self exchange is regulated by beta-adrenergic agents acting via cAMP. The lack of an effect of vasopressin suggests cellular heterogeneity in this response to cAMP.
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PMID:Regulation of chloride self exchange by cAMP in cortical collecting tubule. 301 99

Differential interference contrast microscopy was used in combination with standard electrophysiological techniques in the in vitro perfused mouse medullary thick ascending limb of Henle's loop (MAL) to evaluate the cell volume responses of this nephron segment during and following exposure to hypotonic media and to assess the role of antidiuretic hormone (ADH) and net salt absorption on the associated volume regulatory processes. Reductions in extracellular osmolality by 50 mosmol resulted in rapid increases in cell volume of approximately 20% with or without exposure to ADH. Cell volume recovery (volume-regulatory decrease, VRD) was much slower in the presence, than in the absence, of ADH. This hormone-mediated impairment of the VRD response could be overcome by the abolishment of net salt absorption with luminal 10(-4) M furosemide. An inverse linear relationship was observed between the rates of net salt absorption and VRD, indicating a finite ability of this nephron segment to enhance solute exit mechanisms whether induced by increases in transcellular traffic or by hypotonic cell swelling. Finally, returning to the isotonic media resulted in cell shrinkage under all conditions [+/- ADH and +(ADH and furosemide)] consistent with cell solute loss mediating VRD. However, recovery of cell volume back to the initial isotonic control value [post-VRD volume regulatory increase (VRI)] was only observed in ADH-treated tubules and was independent of net salt absorption. The post-VRD VRI response could be abolished by isohydric CO2-HCO3- removal or by addition of 10(-4) M amiloride to the peritubular medium. The latter results suggest that parallel Na+-H+ and Cl- -HCO3- exchangers located in basolateral membranes mediate the post-VRD VRI response.
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PMID:Hypotonic cell volume regulation in mouse medullary thick ascending limb: effects of ADH. 314 72

The effect of antidiuretic hormone (arginine vasopressin, AVP) on transepithelial Na+, Cl-, K+, Ca2+ and Mg2+ net transports was investigated in medullary (mTAL) and cortical (cTAL) segments of the thick ascending limb (TAL) of mouse nephron, perfused in vitro. Transepithelial net fluxes (JNa+, JCl-, JK+, JCa2+, JMg2+) were determined by electron probe analysis of the collected tubular fluid. Transepithelial potential difference (PDte) and transepithelial resistance (Rte) were measured simultaneously. cTAL segments were bathed and perfused with isoosmolal, HCO3- containing Ringer solutions, mTAL segments were bathed and perfused with isoosmolal HCO3- free Ringer solutions. In cTAL segments, AVP (10(-10) mol.l-1) significantly increased JMg2+ and JCa2+ from 0.39 +/- 0.08 to 0.58 +/- 0.10 and from 0.86 +/- 0.13 to 1.19 +/- 0.15 pmol.min-1 mm-1 respectively. Neither JNa+ nor JCl-, (JNa+: 213 +/- 30 versus 221 +/- 28 pmol.min-1 mm-1, JCl-: 206 +/- 30 versus 220 +/- 23 pmol.min-1 mm-1) nor PDte (13.4 +/- 1.3 mV versus 14.1 +/- 1.9 mV) or Rte (24.6 +/- 6.5 omega cm2 versus 22.6 +/- 6.4 omega cm2) were significantly changed by AVP. No significant effect of AVP on net K+ transport was observed. In mTAL segments, Mg2+ and Ca2+ net transports were close to zero and AVP (10(-10) mol.l-1) elicited no effect. However NaCl net reabsorption was significantly stimulated by the hormone, JNa+ increased from 107 +/- 33 to 148 +/- 30 and JCl- from 121 +/- 33 to 165 +/- 32 pmol.min-1 mm-1.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Differential effects of ADH on sodium, chloride, potassium, calcium and magnesium transport in cortical and medullary thick ascending limbs of mouse nephron. 319 73


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