Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.6.1.3 (ATPase)
65,361 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Cimetidine was more potent 4 hr after a single injection of 25 or 100 mg/kg body wt in increasing gastric pH than other H2 receptor antagonists, ranitidine and famotidine but was less efficient than H+/K(+)-ATPase inhibitors. Omeprazole rose proventricular and gizzard pH at a lower dose than SCH 28080 and Ro 18-5364 (30, 50 and 200 mg/kg body wt, respectively). 2. Proventricular and gizzard pH values were maximal 1 and 4 hr after a single injection of 7.5 mumol/kg body wt omeprazole. Inhibition of acid secretion was maintained for 24 hr after an injection of 100 mumol/kg. 3. H+/K(+)-ATPase activity in vitro was 10 mumol Pi/hr/mg protein in the microsomal fractions of the proventriculus. It was doubled by nigericine and inhibited by SCH 28080. However, western blots by high specific H+/K(+)-ATPase monoclonal antibody 95-A3 and 95-111 recognized a 42 kDa band but hardly exhibited the specific 95 kDa band recognition. 4. Chickens and immature pullets showed a higher H+/K(+)-ATPase activity than laying hens. Calcium level of the diet did not affect the enzyme activity but coarse particles of calcium fed to pullets or laying hens enhanced the H+/K(+)-ATPase activity when compared with ground particles.
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PMID:Gastric acid secretion in the chicken: effect of histamine H2 antagonists and H+/K(+)-ATPase inhibitors on gastro-intestinal pH and of sexual maturity calcium carbonate level and particle size on proventricular H+/K+ ATPase activity. 790 2

We used the microphysiometer, a sensitive extracellular pH sensor, to resolve luminal (or apical) H+ secretion and basolateral release of OH- as well as liberation of acidic metabolites in rabbit gastric glands. Stimulation of glands via the adenosine 3',5'-cyclic monophosphate pathway produced a biphasic change in the extracellular acidification rate (EAR): after an initial transient decrease below the unstimulated baseline (-40.9 +/- 3.4%), the EAR increased to a steady-state maximal plateau (+98.1 +/- 5.3%) within 30 min (n = 37). We interpret the biphasic EAR profile as an initial excess of basolaterally released OH- followed by delayed luminal efflux of simultaneously produced H+. The elevated EAR at steady state reflected liberation of metabolic acid attributed to H(+)-K(+)-ATPase enzymatic activity. The presence of H2-4,4'-diisothiocyanostilbene-2,2'-disulfonic acid prevented OH- release and reduced steady-state EAR. Basolateral OH- release and steady-state EAR were also inhibited by the H(+)-K(+)-ATPase inactivators omeprazole and SCH-28080. Inhibition of Na+/H+ exchange did not reduce steady-state EAR and did not affect apical H+ production, as judged by the accumulation of the weak base aminopyrine. Sodium thiocyanate (1 mM), which short circuits intraluminal H+ accumulation, blocked OH- release, demonstrating its dependence on H(+)-OH- separation at the apical membrane. A computerized model was developed to illustrate how the observed biphasic EAR profile would result from a delayed luminal efflux of H+ due to transitory intraluminal compartmentalization.
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PMID:Direct measurement of extracellular proton flux from isolated gastric glands. 797 8

1. The characteristics of dopamine (D) receptors were studied in kidney using the radiolabelled receptor assay of [3H]-SCH-23390 for D1 and [3H]-sulpiride for D2 receptors during cardiac hypertrophy. Male Sprague-Dawley rats (175-200 g) underwent abdominal aortic constriction above the renal arteries and were studied 28 days thereafter. Sham operated animals without aortic constriction were used as control. 2. Membranes obtained from kidney cortex showed an increase in the number of binding sites (Bmax) of D1 receptors in the aortic banded group. The apparent affinity for the ligand (Kd) was unchanged with D1 receptors, as compared to sham control. Both Bmax and Kd were unchanged for D2 receptors in the aortic banded group. 3. Autoradiographic data further reinforced the findings, showing an increased number of D1 receptors in the kidney at 28 days after abdominal aortic constriction. These changes were associated with an increase in plasma renin activity in the aortic banded group. Further, Na(+)-K(+)-ATPase as measured by fmol of 32Pi released from [gamma-32P]-ATP, was decreased in the kidney cortex of banded animals. 4. Reversal of hypertrophic parameters was observed in the aortic banded group treated for 14 days with SCH 23390 hydrochloride (0.1 mg kg-1 i.p.), a known D1 receptor antagonist. 5. The present study shows an upregulation of renal D1 receptors following abdominal aortic constriction and it is suggested that upregulation of D receptors may be involved in the development of cardiac hypertrophy.
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PMID:Renal D1 receptors, and not D2, are upregulated after aortic constriction and may be involved in cardiac hypertrophy. 798 81

K+ transport mechanisms in epithelial cells isolated from guinea pig distal colon have been studied using 86Rb as a tracer. A transport pathway has been identified that is proposed to be identical to the mechanism mediating transepithelial K+ absorption. Guinea pig colonocytes take up K+ through at least three separate mechanisms: 1) a Na(+)-dependent, ouabain-sensitive influx that is consistent with the Na(+)-K+ pump, 2) a Na(+)-dependent bumetanide-sensitive influx consistent with the Na(+)-K(+)-2Cl- cotransporter, and 3) a Na(+)-independent ouabain-sensitive influx, consistent with an apical colonic K+ pump. These transport mechanisms are sensitive to metabolic inhibition by rotenone and to vanadate, a blocker of type P adenosinetriphosphatase (ATPases). SCH-28080, an inhibitor of gastric K(+)-H(+)-ATPase, was without effect. Measurements of net K+ fluxes revealed that isolated colonocytes concentrated K+ by two processes: 1) a Na(+)-dependent ouabain-sensitive mechanism, which is compatible with the Na(+)-K+ pump and 2) a Na(+)-independent ouabain-sensitive mechanism consistent with the proposed absorptive K+ pump. These concentrative mechanisms were also inhibited by rotenone and vanadate, but not by SCH-28080. The Na(+)-independent ouabain-sensitive K+ pump was present in the distal colon, but absent in the proximal colon and the small intestine of guinea pig. It is proposed that this Na(+)-independent ouabain-sensitive K+ pump mediates K+ absorption and is related to the luminal K(+)-ATPase.
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PMID:K+ transport in isolated guinea pig colonocytes: evidence for Na(+)-independent ouabain-sensitive K+ pump. 802 40

Colonocytes must regulate intracellular pH (pHi) while they transport H+ and HCO3-. To investigate the membrane transport processes involved in pHi regulation, colonocyte pHi was measured with 2,'7'-bis(2-carboxyethyl)-5(6)-carboxyfluorescein (BCECF) in intact segments of rat distal colon mounted on a holder that fits into a standard fluorometer cuvette and allows independent superfusion of mucosal and serosal surfaces. When NCECF-acetoxymethyl ester was in the mucosal solution only, BCECF loaded surface colonocytes with a high degree of selectivity. In HEPES-buffered solutions, basal pHi was 7.31 +/- 0.01 (n = 68), and pHi was dependent on extracellular Na+. Cells acidified in Na(+)-free solution, and pHi rapidly corrected when Na+ was returned. pHi recovered at 0.22 +/- 0.01 pH/min (n = 6) when Na+ was introduced into the mucosal solution and at 0.02 +/- 0.01 pH/min (n = 7) when Na+ was absent from the mucosal solution. The presence or absence of Na+ in the serosal solution did not affect pHi. This indicated that the Na(+)-dependent pHi recovery process is located in the apical cell membrane, but not in the basolateral membrane. Because amiloride (1 mM) inhibited Na(+)-dependent pHi recovery by 75%, Na+/H+ exchange appears to be present in the apical membrane. Because Na(+)-independent pHi recovery was not affected by K(+)-free media, 50 microM SCH-28080, 100 nM bafilomycin A1, or Cl(-)-free media, this transport mechanism does not involve a gastriclike H(+)-K(+)-ATPase, a vacuolar H(+)-ATPase, or a Cl-/base exchanger. In summary, pHi was selectively measured in surface colonocytes by this technique. In these cells, the Na+/H+ exchange activity involved in pHi regulation was detected in the apical membrane, but not in the basolateral membrane.
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PMID:Identification of Na+/H+ exchange on the apical side of surface colonocytes using BCECF. 804 24

We stably expressed the rat D1A dopamine receptor in mouse fibroblast LTK- cells and obtained specific ligand binding and functional activity characteristic of the D1A dopamine receptor coupled to stimulation of adenylyl cyclase. In the transfected cells, the selective D1 agonist fenoldopam caused a concentration-dependent inhibition of Na+/K(+)-ATPase activity, achieving maximum inhibition of approximately 30%. The latter was abolished by the selective D1 antagonist (+)-SCH 23390 and by the specific protein kinase A inhibitor protein kinase inhibitor-(6-22) amide. In the nontransfected cells, fenoldopam did not affect Na+/K(+)-ATPase activity. 8-Chlorophenylthio-cAMP inhibited Na+/K(+)-ATPase activity in both transfected and nontransfected cells; this effect was blocked by protein kinase inhibitor-(6-22). These results indicate that the inhibition of Na+/K(+)-ATPase activity induced by agonist occupancy of D1A receptors is mediated by protein kinase A.
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PMID:D1A dopamine receptor stimulation inhibits Na+/K(+)-ATPase activity through protein kinase A. 809 27

Endogenous kidney dopamine (DA) causes natriuresis and diuresis, at least partly, via inhibition of proximal tubular Na+,K(+)-ATPase. The present study was done to identify the dopamine receptor subtype(s) involved in dopamine-induced inhibition of Na+,K(+)-ATPase activity. Suspensions of renal proximal tubules from Sprague-Dawley rats were incubated with dopamine, the DA-1 receptor agonist fenoldopam or the DA-2 receptor agonist SK&F 89124 in the presence or absence of either the DA-1 receptor antagonist SCH 23390 or the DA-2 receptor antagonist domperidone. Dopamine and fenoldopam (10(-5) to 10(-8) mol/l) produced a concentration-dependent inhibition of Na+,K(+)-ATPase activity. However, SK&F 89124 failed to produce any significant effect over the same concentration range. Incubation with fenoldopam (10(-5) to 10(-8) mol/l) in the presence of SK&F 89124 (10(-6) mol/l) inhibited Na+,K(+)-ATPase activity to a degree similar to that with fenoldopam alone. Furthermore, DA-induced inhibition of Na+,K(+)-ATPase activity was attenuated by SCH 23390, but not by domperidone. Since alpha-adrenoceptor activation is reported to stimulate Na+,K(+)-ATPase activity and, at higher concentrations, dopamine also acts as an alpha-adrenoceptor agonist, the potential opposing effect from alpha-adrenoceptor activation on DA-induced inhibition of Na+,K(+)-ATPase activity was investigated by using the alpha-adrenoceptor blocker phentolamine. We found that, in the lower concentration range (10(-5) to 10(-7) mol/l), dopamine-induced inhibition of Na+,K(+)-ATPase activity in the presence of phentolamine was similar in magnitude to that observed with dopamine alone.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Inhibition of Na+,K(+)-ATPase in rat renal proximal tubules by dopamine involved DA-1 receptor activation. 809 67

Recently, we have shown that polarization of an electrogenic H+/K(+)-ATPase pump located in the secretory (luminal) membrane of the frog gastric mucosa is the major factor contributing to the increase in open circuit potential difference (OCPD) induced by voltage clamping. While this transmucosal polarization was not affected by removal of Cl- and Na+ and minimally affected by increasing the K+ concentration to 79 mM in both nutrient and secretory solutions, it was markedly reduced by 10(-3) M famotidine (beta blocker) or 10(-4) M omeprazole (H+/K(+)-ATPase inhibitor) in the nutrient solution. In present experiments, the effects of three other inhibitors of H+ secretion were examined, namely, cimetidine (beta blocker), SCH 28,080 (H+/K(+)-ATPase inhibitor) and SCN- (non-specific inhibitor). While cimetidine and SCH 28,080 markedly reduced the polarization induced by voltage clamp, SCN- affected the polarization to a lesser extent. These data further support the electrogenicity of the frog gastric mucosa proton pump and the lack of a direct effect of SCN- on the pump.
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PMID:Electrogenicity of the frog gastric mucosa proton pump based on polarization responses in the presence of H(+)-secretion inhibitors. 832 38

Cells from RCCT-28A cell line, which exhibited the highest peanut-lectin binding capacity [RCCT-28A(P+)] were separated and cultured attempting to obtain a population of HCO3- secreting cells. The mechanisms of apical solution acid or base extrusion were studied in confluent monolayers. In RCCT-28A (P+) cells net H+ flux (JH+, nmol.min-1.cm-2) was significantly lower (JH+ = 13 +/- 3) than that observed in the RCCT-28A cells (21 +/- 2). N-ethylmaleimide, Bafilomycin-A, omeprazole and Schering 28080 decreased JH+. Cl- removal from the basolateral side, in the presence or absence of SCH in the apical side, decreased JH+. Removal of apical Cl- abolished apical extrusion of base-equivalents. Incubation in a high bicarbonate solution results in base-equivalent flux to the apical side (JH+ = -7.0 +/- 1.0). Preincubation in a hyperosmotic medium (mannitol addition) at pH 7.5 decreased JH+ to -3.0 +/- 1.0. We conclude that, functionally, RCCT-28A(P+) cells are only quantitatively different from RCCT-28A cells. Acid secretion by these cells can be modulated by alkaline and by hyperosmolar preincubation and is most likely mediated by coexistent of apical H(+)-ATPase and H+,K(+)-ATPase. The main mechanism of net OH- secretion appears to be Cl-/HCO3- exchange at the apical side.
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PMID:Characterization of peanut-lectin (+) cells derived from the RCCT-28A cell line. 838 90

Dopamine (DA) stimulated K+ efflux (assessed as 86Rb+ efflux) in retinal suspensions of posthatched chicken. This effect was dose dependent (EC50 = 22 microM), was mimicked by the D1-selective agonist SKF-38393, and reversed by the D1-selective antagonist SCH-23390, indicating an involvement of D1 receptors. Analogues of cyclic AMP (cAMP) did not mimic the DA action. Moreover, DA failed to affect cAMP levels, suggesting that adenylyl cyclase (AC) was not involved. In contrast, forskolin (FSK) stimulated both K+ efflux and cAMP accumulation in the retina (EC50 of 10 microM for both effects). The FSK-elicited K+ efflux was not mimicked by 1,9-dideoxy-FSK (an analogue of FSK that does not activate AC), suggesting that FSK stimulated K+ efflux through the activation of AC. Both DA and FSK inhibited Na+,K(+)-ATPase activity in the retina. However, the DA-elicited K+ efflux was independent of this inhibition, whereas the FSK effect on K+ efflux was largely due to the inhibitory action of the diterpene of the ion pump. A possible role of protein kinase C (PKC) in the DA action was explored. The PKC activator 4 beta-phorbol 12-myristate 13-acetate (4 beta-PMA) potently (EC50 = 4 nM) stimulated K+ efflux. This action was not mimicked by the inactive isomer 4 alpha-PMA. When added together, DA and 4 beta-PMA behaved in an additive manner, suggesting separate mechanisms of action for these two drugs. Moreover, DA failed to stimulate retinal phosphoinositide hydrolysis, a well-known pathway leading to PKC activation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Dopamine stimulates K+ efflux in the chick retina via D1 receptors independently of adenylyl cyclase activation. 839 94


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