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 rat cortical collecting duct (CCD) exhibits high rates of NaCl reabsorption when stimulated by mineralocorticoid and antidiuretic hormone (ADH). The present study was undertaken to determine if there is significant transcellular Cl- movement across the principal cells of the rat CCD. CCDs were dissected from kidneys of rats that had been injected with deoxycorticosterone (5 mg, i.m.) 2-9 days prior to the experiment. The ducts were perfused in vitro with identical perfusing and bathing solutions, except that 200 pmol.l-1 ADH was added to the bathing solutions. The basolateral membrane voltage (PDbl) of principal cells was -77 +/- 1 mV and the luminal membrane voltage (PD1) was -68 +/- 1 mV (mean +/- SEM, n = 124). Separate impalements with single-barrelled Cl(-)-selective microelectrodes gave an apparent intracellular Cl- activity of principal cells of 17 +/- 2 mmol.l-1. Transepithelial PD and PDbl were unaffected by luminal furosemide, hydrochlorothiazide (HCT), 4-acetamido-4-isothiocyanostilbene2,2-disulphonic acid, (SITS), or the Cl- channel blocker 5-nitro-2-(3-phenylpropylamino)-benzoic acid (NPPB); bath addition of SITS or the Cl- channel blocker diphenylamino-2-carboxylic acid; or replacement of bath HCO3- by Cl-. The intracellular Cl- activity (a(cell)Cl) also remained unchanged with the addition of HCT, SITS or the Cl- channel blockers to either the perfusing or bathing solutions, or with replacement of the bathing solution HCO3-.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Principal cells of cortical collecting ducts of the rat are not a route of transepithelial Cl- transport. 227 16

In a previous study (Watts et al., '87) we reexamined the projections of the suprachiasmatic nucleus (SCh) with the PHA-L method and found that they could be divided conveniently into six groups of fibers. By far the densest projection ends just dorsal to the SCh in a comma-shaped region designated the "subparaventricular zone," although some fibers continue on through the paraventricular nucleus of the hypothalamus to end in the overlying midline thalamus, and others continue on to end in the dorsomedial nucleus, the region around the ventromedial nucleus, and the posterior hypothalamic area. Other relatively sparse projections from the SCh were also described to the preoptic region, lateral septal nucleus, parataenial and paraventricular nuclei of the thalamus, and ventral lateral geniculate nucleus. In addition, the same method was used to show that the subparaventricular zone projects in turn massively to these same regions, as well as back to the SCh itself and to the periaqueductal gray. The present series of experiments was designed to confirm these observations with retrograde tracer injections and to investigate the cellular and possible neurotransmitter organization of the major projections from the SCh and subparaventricular zone with a combined retrograde tracer-immunohistochemical method. For this, the distribution of neuronal cell bodies within the SCh that stain with antisera to vasopressin, vasoactive intestinal polypeptide (VIP), corticotropin-releasing factor, bombesin, substance P, neurotensin, somatostatin, thyrotropin-releasing hormone, and angiotensin II was described in detail first. Then the distribution of retrogradely labeled neurons that were also stained for one or another of these peptides was described after injections of true blue, or in some cases SITS, into the regions of the subparaventricular zone, the paraventricular and parataenial nuclei of the thalamus, the ventromedial nucleus, the dorsomedial nucleus, and the periaqueductal gray. The results confirm previous immunohistochemical and anterograde tracing studies and in addition indicate that cells in dorsal as well as ventral parts of the SCh project to each of the terminal fields examined, as do many cells in surrounding areas, including the subparaventricular zone. Our results also suggest that, at the very least, vasopressin-, VIP-, and neurotensin-stained cells in the SCh project to the subparaventricular zone, midline thalamus, and dorsomedial nucleus, and that the vasopressin and VIP-stained fiber systems are partially segregated at the level of the subparaventricular zone.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Efferent projections of the suprachiasmatic nucleus: II. Studies using retrograde transport of fluorescent dyes and simultaneous peptide immunohistochemistry in the rat. 243 9

1--The mechanism of the vasopressin-induced, facilitated transport across toad urinary bladder was studied by treating the luminal membrane of the epithelium with the following reagents of protein functional groups: NEM (SH groups), SITS (amino groups), EEDQ (carboxylic groups), DEPC (histidine). 2--Treatment of the luminal side of the epithelium by NEM strongly inhibits the ADH-induced urea transport, leaving unmodified the effect of the hormone on the flux of antipyrine, a lipid soluble molecule. These results confirm the hypothesis that the urea carrier is of proteic nature. 3--Treatment of the luminal side by SITS strongly inhibits ADH action on urea and antipyrine permeability; thus this effect can be considered rather unspecific. 4--On the contrary the EEDQ effect is more specific; in fact treatment of the luminal side by EEDQ strongly inhibits ADH effect on the permeability of urea, slightly increasing the ADH effect on that of antipyrine. 5--Finally, the luminal treatment by diethylpyrocarbonate inhibits almost completely the ADH action on the urea fluxes, slightly increasing the hormone effect on the antipyrine ones. 6--Based on these results we conclude that carboxylic groups and the imidazolic ring are more important than the amino groups in determining the urea transport across toad bladder, in the presence of ADH.
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PMID:Effect of reagents of protein functional groups on the ADH-induced urea facilitated transport across toad urinary bladder. 245 74

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

Acidification of the medium bathing the serosal surface of the toad urinary bladder results in impairment of the water permeability response to vasopressin. The magnitude of the hydrosmotic response to a maximal concentration of either vasopressin or the cyclic nucleotide analogue 8-(p-chlorophenylthio)-cyclic 3',5'-adenosine monophosphate (C1PhS-cAMP) was progressively reduced when serosal bath pH was decreased from 8.5 to 6.5. The disulfonic stilbenes SITS and DIDS and the diuretic furosemide, agents known to interfere with anion transport and with the regulation of intracellular pH in other tissues, inhibited the water flow response to vasopressin and C1PhS-cAMP in a pH-dependent manner when added to the serosal bathing medium. Inhibition of the hydrosmotic response to 10(-5) M C1PhS-cAMP was estimated to be half-maximal at 1.5 X 10(-4) M SITS, 2 X 10(-5) M DIDS, and 1 X 10(-5) M furosemide. The degree of inhibition induced by the anion transport inhibitors varied inversely with the concentration of exogenous cyclic nucleotide. SITS, DIDS, and furosemide had no effect on either basal or vasopressin-stimulated short-circuit current at serosal pH 8.5; all three agents inhibited basal short-circuit current at pH 7.1 but had no effect on the natriferic response to vasopressin. These results are consistent with the view that changes in intracellular hydrogen ion and/or anion concentration can selectively inhibit the increase in water permeability elicited by vasopressin at a step(s) distal to the generation of cAMP.
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PMID:Anion transport inhibitors: effects on water and sodium transport in the toad urinary bladder. 298 47

1. The effects of Na+ on vasopressin release and on redistribution of Ca2+, Na+ and H+ in isolated rat neurohypophysial nerve endings have been studied. 2. Substituting Na+ for a non-permanent cation produced a pronounced and sustained release of vasopressin. This increase occurred in the absence of external Ca2+ and in nerve endings loaded with the Ca2+ chelator dimethyl-BAPTA (1,2-bis-(O-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid). 3. The effect of Na+ was independent of a rise in intracellular Ca2+ as judged by the measurement of [Ca2+]i using the indicator fura-2 and 45Ca2+ efflux studies. Although Na+ could release Ca2+ from internal reservoirs the small elevation in [Ca2+]i induced by Na+ could not explain the large and sustained increase in vasopressin secretion. 4. The channel blockers TTX (tetrodotoxin), D888 (desmethyoxyverapamil), N144 (5-nitro-2-(phenylpropylamino)-benzoic acid) or SITS (4-acetamido-4'-isothiocyanatostilbene-2,2'-disulphonic acid) could not prevent the Na(+)-dependent increase in vasopressin release. Similarly this increase was not affected by metabolic inhibitors (Ruthenium Red and KCN) nor by CCCP (carbonyl cyanide m-chlorophenylhydrazone), an uncoupler of oxidative phosphorylation. 5. Selectivity among monovalent cations to promote secretion was found with the largest effect on the secretory response being produced by Na+. Similarly Cl- was found to be the most potent anion studied for inducing, in the presence of Na+, an increase in neurohormone release. 6. Measuring [Na+]i by means of the Na+ indicator SBFI showed that the extent of the secretory response was correlated with the intraterminal Na+ concentration. 7. The Na(+)-induced, Ca(2+)-independent release of vasopressin occurred by exocytosis as judged (i) by the linear relationship between the amount of vasopressin secreted and that of the co-localized neurophysin and (ii) by the demonstration that the extracellular marker horseradish peroxidase was only found in endocytotic vacuoles and not in the cytoplasm of the stimulated nerve endings. 8. The Na(+)-dependent secretory response found on addition of extracellular Na+ was not the result of the change in internal pH as measured with the indicator BCECF and as mimicked by addition of propionic acid. 9. Addition of Na+ to digitonin- or streptolysin-O-permeabilized nerve endings in the presence or absence of Ca2+ also gave rise to an increase in vasopressin secretion. 10. It is concluded that an increase in internal Na+ per se can promote, in the absence of a rise in intracellular Ca2+, an increase in neuropeptide secretion.
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PMID:Sodium-evoked, calcium-independent vasopressin release from rat isolated neurohypophysial nerve endings. 750 28

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