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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Calcium salts were found to replace ACTH in inducing steroidogenesis in isolated adrenocortical cells from rats. This Ca-specific stimulation occurred when the cation was presented to the cells in the presence of phosphate and carbonate as a counter-ions under conditions which favoured the formation of colloidal calcium. Colloid generation and stabilization was facilitated by the use of calcium buffers and gelatin. Stable soluble or sparingly soluble calcium complexes were inactive. The preparation of cells and metastable calcium solutions is described in detail. The Ca trigger was sensitive to Ca deprivation or inhibitors of Ca transport and could be replced by Sr. The relative role of Ca and cyclic AMP as second messengers is discussed.
Mol Cell Endocrinol 1978 Jan
PMID:Steroidogenesis in isolated adrenal cells: excitation by calcium. 20

Compounds were studied that inhibit the oxidative degradation of human serum albumin by peroxidase and the enzyme model, iron hydroxide. Differences between the two oxidants gave clues for the mechanism of inhibition. The inhibitors studied were inorganic anions, phosphate, sulfate, carbonate and molybdate; organic anions, decanoate and glycocholate; and the nonionic species, glycogen. Such inhibitors might be considered as adjuvants in senescence: by decreasing the rate of enzymic oxidation of essential body proteins, they would, in the course of aging, reduce some of the physiological changes occurring as a result of accumulation of degraded protein.
Mol Biol Rep 1979 Feb 15
PMID:Inhibitors of oxidative degradation of protein: gerontological implications. 44 Feb 99

The condensation products obtained from 0.01M S-glycyl-N-acetyl-cysteamine at different pH's were investigated. The highest yields of diketopiperazine (approx. 50%) were observed in phosphate buffers between pH 7.5 and 8.5. The highest yields of diglycine (46%), triglycine (10%) and tetraglycine (2%) were observed in carbonate buffers at pH 9.5. At pH 8.0, over 90% of the glycyl residues of 0.15M S-glycyl-N-acetylcysteamine were incorporated into condensation products, mainly DKP (60--70%). The yields of products from the condensation of S-glycyl-ethanethiol under similar conditions closely resembled those obtained with S-glycyl-N-acetylcysteamine.
J Mol Evol 1979 Oct
PMID:The formation of peptides from glycine thioesters. 50 43

1. Acute chloride depletion, without sodium depletion, was produced in rats by a single exchange peritoneal dialysis against sodium bicarbonate solution. Blood volume was restored after dialysis by infusion of salt-free albumin, and exogenous deoxycorticosterone and antidiuretic hormone were given. 2. Clearance studies in the period (3 h) after dialysis revealed no difference in the glomerular filtration rate or in the filtered sodium load between experimental and control rats but urinary sodium concentrations and absolute and fractional sodium excretion were significantly higher in the chloride-depleted group. 3. There was also a significant kaliuresis, increased urinary flow rate and diminished free water reabsorption. Urinary bicarbonate excretion increased to a variable degree but the major rise in anion excretion was 'unmeasured' (Na+ + K+ - [Cl- + HCO3- + PO4(3-)]). 4. It is postulated that chloride depletion imposes limitations on sodium reabsorption in the ascending limb of the loop of Henle.
Clin Sci Mol Med 1977 Jan
PMID:Natriuresis in rats acutely depleted of chloride. 60 61

1. Chemical and morphological features of uraemic bone disease were studied by comparison of bone composition in 44 patients with uraemia (12 dialysed and 32 non-dialysed) and 36 control subjects. The significant changes included decreased bone mineral carbonate associated with calcium, a concomitant increase in phosphate, and an increase in magnesium. There was also an increase in osteoid and a reduction in the specific gravity of the compact bone. 2. The most marked changes in bone composition were observed in patients with uraemia of more than 1 year's duration, who had been dialysed. Bone mineral sodium concentrations were not significantly altered in any group. 3. The changes in bone mineral composition appeared to be the result of several simultaneous and/or successive mechanisms: (i) loss of fixed base, calcium carbonate; (ii) replacement of carbonate by phosphate; (iii) the addition of immature bone mineral, which contains high concentrations of phosphate and relatively low concentrations of carbonate. 4. These observations are consistent with earlier views of the bone salt as an indefinite calcium/phosphate/carbonate complex. Variations in bone composition may arise from a reciprocal relationship between phosphate and carbonate. The bone mineral analogue that best explains these variations in bone composition is octacalcium phosphate carbonate [Ca4 (PO4)2(HPO4)x(CO3)1-x,zH2O].
Clin Sci Mol Med 1977 Oct
PMID:Inter-relationships of carbonate, phosphate, monohydrogen phosphate, calcium, magnesium and sodium in uraemic bone: comparison of dialysed and non-dialysed patients. 91 54

1. The effects of pent-4-enoic acid, an inhibitor of fatty acid oxidation, were studied in dogs undergoing water diuresis and acetazolamide diuresis. Free water excretion and distal solute delivery were increased when infusion of pent-4-enoic acid was superimposed on an increasing mannitol diuresis. 2. Bicarbonate excretion increased significantly when infusion of pent-4-enoic acid was superimposed on maximum acetazolamide diuresis. 3. Phosphate excretion exceeded 90% of filtered load when pent-4-enoic acid was administered under stable free water conditions and increased significantly when pent-4-enoic acid was superimposed on stable acetazolamide diuresis. 4. The results are interpreted as indicating inhibition of proximal tubular reabsorption by pent-4-enoic acid, emphasizing the importance of fatty acids as a major fuel for proximal tubular metabolism.
Clin Sci Mol Med 1975 Nov
PMID:Effects of pent-4-enoic acid on renal free water, bicarbonate and phosphate excretion in the dog. 119 98

Stimulation with extracellular ATP causes a rapid initial transient rise followed by asynchronous periodic oscillations in cytosolic calcium ion activity ([Ca2+]i) in individual aortic smooth muscle cells in either HEPES-buffered or HCO3(-)-buffered saline. The dose at which one-half of the cells display an initial rise in cytosolic calcium is 0.11 microM ATP in the presence of external Ca2+ and 0.88 microM ATP in the absence of external Ca2+; the corresponding value for oscillations in the presence of external Ca2+ is 2.6 microM ATP. While the initial transient displays rapid desensitization, the oscillations persist for greater than 30 min in the continuous presence of ATP. The presence of the agonist ATP is also absolutely required for the maintenance of the oscillations, presumably to provide continuous activation of P2 purinoceptors. The average frequency of oscillation is approximately 0.9 min-1. The frequency depends only slightly on the concentration of ATP, and oscillations do not collapse into a prolonged elevated [Ca2+]i at high concentrations of ATP. Both Ca2+ influx and release from internal stores participate in the initial transient. Oscillations are not produced in the absence of external Ca2+ but are initiated upon the addition of external Ca2+ in the continued presence of ATP. Oscillations in progress are abolished by the removal of extracellular Ca2+ with one additional peak occurring after the Ca2+ removal. These data suggest that extracellular Ca2+ influx is required for the maintenance of the posttransient oscillations, presumably to provide the Ca2+ necessary for refilling intracellular Ca2+ pools that are the source of the oscillating [Ca2+]i. The Ca2+ influx is not regulated by voltage-gated Ca2+ channels. The data in this report are consistent with the view that the initial transient has contributions from two receptor-mediated pathways, and the oscillations are controlled either by a mechanism separate from the ones that control the initial transient or by steps whose control diverges before the point of desensitization.
Mol Biol Cell 1992 May
PMID:Independent pathways regulate the cytosolic [Ca2+] initial transient and subsequent oscillations in individual cultured arterial smooth muscle cells responding to extracellular ATP. 131 42

pH is maintained in cells by plasma membrane exchange mechanisms. In the absence of HCO3- ions, FRTL-5 cells regulate intracellular pH (pHi) by an Na+/H+ antiport but HCO3(-)-dependent exchangers cannot operate. We have investigated pHi regulation (by microfluorimetry and the pH sensitive dye 2',7'-bis(2-carboxyethyl)-5(6')-carboxyfluorescein) in small groups (five to six cells) of FRTL-5 thyroid cell monolayers held in Krebs-Ringer buffer (pH 7.4) with or without HCO3- ions. The exchangers were investigated with inhibitors (amiloride or its derivative dimethylamiloride for the Na+/H+ antiporter and the stilbene derivative disodium 4,4'-diisothiocyanatostilbene-2,2'-disulphonic acid (DIDS) for HCO3(-)-dependent mechanisms), ionic substitution and by NH4+/NH3 (10 mM) acid loading. Basal pHi was lower in the presence (7.3 +/- 0.058, mean +/- S.D., n = 14) than in the absence (7.59 +/- 0.078, n = 10) of HCO3- ions. In HCO3(-)-free media, cells recovered from acid load by 0.34 +/- 0.04 pH units in the first 2 min and finally reached a pHi of 7.35 +/- 0.06. This recovery was Na(+)-dependent and blocked by dimethylamiloride during the 15 min following intracellular acidification. In HCO3(-)-containing media, cells recovered from an acid load at a similar rate, but reached 99 +/- 10% (n = 9) of the baseline pH; this recovery was also dependent on Na+ ions. Moreover, although dimethylamiloride and DIDS reduced the rate of recovery to 0.06 +/- 0.02 and 0.18 +/- 0.04 pH units respectively during the 2-min period, the cells returned to the basal pHi within 15 min.(ABSTRACT TRUNCATED AT 250 WORDS)
J Mol Endocrinol 1992 Dec
PMID:Identification of exchange mechanisms for the regulation of intracellular pH in rat thyroid FRTL-5 cells. 133 27

Vascular smooth muscle intracellular pH is maintained by the Na+/H+ and Cl-/HCO3- antiporters. The Na+/H+ exchanger is a major route of H+ extrusion in most eukaryotic cells and is present in vascular smooth muscle cells in a similar capacity. It extrudes H+ into the extracellular space in exchange for Na+. The Cl-/HCO3- exchanger plays an analogous role to lower the pH of vascular smooth muscle cells when increases in intracellular pH occur. Its activity has also been demonstrated in A7r5 and A10 vascular smooth muscle cells. The Na+/H+ exchanger is regulated by a number of agents which act through inositol trisphosphate/diacylglycerol, to stimulate the antiporter. Calcium-calmodulin dependent protein kinase may also activate the antiporter in vivo. Phosphorylation of the Cl-/HCO3- exchanger has also been observed but its physiological role is not known. Both these antiporters exist in the plasma membrane as integral proteins with free acidic cytoplasmic termini. These regions may be important in 'sensing' changes in intracellular pH, to which these antiporters respond.
Mol Cell Biochem 1991 Apr 10
PMID:The role of ion antiporters in the maintenance of intracellular pH in rat vascular smooth muscle cells. 165 79

In blood vessels in the systemic circulation, the plasmalemmal Na+/H+ exchanger has been implicated in a variety of cellular functions, including the regulation of intracellular pH (pHi) and cell volume, and the response to smooth muscle mitogens. The role of this transport system in pulmonary vascular smooth muscle has not been explored. The present study examined the characteristics of Na+/H+ exchange in cultured guinea pig pulmonary artery smooth muscle cells. These cells were subjected to an acid load, and the recovery from acid loading was monitored using the fluorescent pH-sensitive dye 2',7'-bis(carboxyethyl)-5(6)-carboxyfluorescein (BCECF). In the absence of HCO3-, pHi recovery from acid loading was dependent on external Na+ and was inhibited by the Na+/H+ exchange inhibitor dimethylamiloride (DMA) (recovery rate was reduced from 54.4 +/- 5.5 to 12.8 +/- 2.0 mmol H+/liter.min). This exchanger was also active in the presence of HCO3-; DMA reduced resting pHi and slowed the rate of recovery from acid loading in HCO3- buffers. However, in the presence of HCO3-, other transport systems, presumably HCO3-/Cl- exchange, also contribute to the regulation of pHi. In HCO3- buffers, the rate of recovery from acid load averaged 40.8 +/- 1.8 mmol H+/liter.min. Addition of 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS), an inhibitor of HCO3-/Cl- exchange, slowed this recovery to 25.5 +/- 1.6 mmol H+/liter.min. A combination of DIDS and DMA further slowed the recovery to 19.7 +/- 1.5 mmol H+/liter.min. These findings indicate that the Na+/H+ exchanger plays a significant role in the regulation of pHi in pulmonary artery smooth muscle cells, even in HCO(3-)-containing buffers.
Am J Respir Cell Mol Biol 1991 Dec
PMID:Contribution of Na+/H+ exchange to pH regulation in pulmonary artery smooth muscle cells. 165 36


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