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. The output of acetylcholine from the plexus of the guinea-pig ileum longitudinal strip has been used to study the mechanism of acetylcholine release. From the effects of hexamethonium and tetrodotoxin, it was inferred that 60% of the normal resting output is due to propagated activity in the plexus, and 40% to spontaneous release. Tetrodotoxin virtually abolishes the increase in output in response to electrical stimulation.2. Resting acetylcholine output is increased when the bathing medium is changed in the following ways:(a) sodium replacement by sucrose, trometamol or lithium;(b) addition of ouabain or p-hydroxymercuribenzoate (PHMB), or withdrawal of potassium;(c) the combination of PHMB and partial sodium replacement;(d) addition of potassium; this increase in output becomes greater in the absence of sodium.3. The resting output is virtually abolished by calcium withdrawal, and is restored by barium substitution for calcium. It is also reduced by raising the magnesium concentration.4. The enhanced resting output in response to sodium withdrawal also occurs in the absence of calcium.5. Cooling to 5 degrees C greatly reduces both the resting output and the output in response to raised potassium concentration or to electrical stimulation.6. The increase in resting output due to potassium excess is slight up to 25 mM [K(+)](o), but increases thereafter with about the fourth power of the potassium concentration; it is resistant to tetrodotoxin.7. Synthesis of acetylcholine by the longitudinal strip is increased when output is enhanced by electrical stimulation, by potassium excess or by addition of barium, so that the acetylcholine content of the strip is maintained approximately normal. Synthesis is reduced, in relation to output, by potassium lack or by treatment with ouabain, and is virtually abolished by sodium withdrawal.8. The theory is discussed that acetylcholine release depends on inhibition of the activity of a (Na(+) + K(+) + Mg(2+))-activated ATPase at the axonal membrane.
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PMID:The mechanism of acetylcholine release from parasympathetic nerves. 425 76

1. Spleen slices pre-incubated for different periods at 4 degrees C in Krebs solution containing varying concentrations of calcium, up to 96 mM, lost their endogenous noradrenaline stores when reincubated in normal Krebs solution at 37 degrees C for 2 hr. Rate of loss of noradrenaline was roughly related to the calcium concentration of the pre-incubation medium and the pre-exposure time.2. Pre-treatment with isotonic barium or strontium (96 mM) Krebs solution also induced release of noradrenaline from spleen slices when re-exposed to normal Krebs solution. Barium was more effective than either calcium or strontium.3. The enhanced release induced by calcium pre-treatment occurred in the absence of calcium, with or without EGTA.4. Tissue calcium concentration of spleen slices was 0.68 m-mole/kg. Pre-treatment of slices with normal or 96 mM calcium-Krebs solution for 4 hr at 4 degrees C increased the calcium concentration to 2.57 and 9.9 m-mole/kg, respectively.5. Ouabain, which caused a dose-dependent release of noradrenaline, did not modify the release induced by calcium pre-treatment.6. Spleen slices prepared from cats anaesthetized with sodium pentobarbitone instead of ether were resistant to noradrenaline depletion by calcium pre-treatment.7. Evoked release of [(3)H]noradrenaline by high potassium from calcium-pre-treated slices did not occur in the absence of external calcium, even though the calcium pre-treatment enhanced the tissue concentration of this ion by nearly tenfold.8. Net uptake of noradrenaline in normal and in treated slices whose noradrenaline content was severely reduced by barium pre-treatment or sodium withdrawal was comparable.9. Specific activity of released and endogenous [(3)H]noradrenaline increased as the tissue stores of noradrenaline were reduced.10. It is suggested that the spontaneous loss of tissue noradrenaline after pre-treatment with high-calcium solution was due to inhibition of sodium-potassium-activated ATPase by intracellular accumulation of calcium ions. Evidence is presented to suggest that vesicles depleted of their endogenous transmitter by pre-treatment with calcium, strontium or barium, or by sodium withdrawal, are re-used for the storage and release of exogenous noradrenaline.
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PMID:Release of noradrenaline from slices of cat spleen by pre-treatment with calcium, strontium and barium. 477 3

Active sodium absorption by a variety of epithelia is abolished by ouabain, but the obligatory coupling between the movement of sodium and potassium expected from a basolateral (Na+ + K+) ATPase has not been convincingly demonstrated. According to the model of Koefoed-Johnsen and Ussing, the asymmetric cation selectivities of the apical and basolateral membranes prevent basolateral Na-K exchange from being expressed as opposing transmural ion flows. An additional consequence of this asymmetry is that the short-circuit current (Isc) cannot be identified with the current through the sodium-potassium pump. We used the polyene antibiotic, amphotericin-B, to reduce the resistance and the cation selectivity of the apical membrane of isolated turtle colon so that the basolateral membrane current could be dissected into two components: one through a barium-sensitive potassium channel and another which represents the current associated with ouabain-sensitive, electrogenic, Na-K exchange. Comparison of cation fluxes and short circuit current indicates that in these conditions active sodium absorption is entirely attributable to an electrogenic Na-K pump with a stoichiometry of approximately 3Na:2K.
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PMID:Active sodium transport by turtle colon via an electrogenic Na-K exchange pump. 625 98

1. The role of Na+-K+-activated ATPase in the regulation of resistance vessel reactivity to barium chloride and noradrenaline was investigated with a pair-perfused hindquarter technique in spontaneously hypertensive rats and Wistar-Kyoto rats (6 and 12 week old). Ouabain (10(-4) mol/l) was used to inhibit the sodium pump. 2. In all groups studied, dose-response curves to agonists were shifted to the left when ouabain was added to the perfusion medium. This potentiation in vascular reactivity produced by ouabain was expressed as 'index for sodium-pump inhibition' (ISPI = ED 50 of an agonist/ED50 + ouabain). 3. In mature rats index for sodium-pump inhibition calculated for both agonists was significantly greater in spontaneously hypertensive rats in comparison with Wistar-Kyoto rats, but not so in young spontaneously hypertensive rats. There was, however, a trend towards increased noradrenaline sensitivity in spontaneously hypertensive rats although the difference from Wistar-Kyoto rats was not statistically significant. 4. The data may suggest that there is some increase in the activity of the sodium pump in the resistance vessels of mature spontaneously hypertensive rats, perhaps to compensate for an increased passive sodium permeability.
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PMID:Studies on the role of sodium-potassium-activated ATPase as determinant of vascular reactivity in Wistar-Kyoto and spontaneously hypertensive rats. 625 13

Two models ('single-pump' and 'two-pump') of transepithelial potassium movement by the marginal cells of the stria vascularis have been proposed in the literature. Their validity was considered by exposing the endolymphatic (luminal) surface to agents (barium, valinomycin and nystatin) which are known to alter specific cellular membrane conductances in other tissues. This was accomplished by the use either of injections or of a relatively satisfactory technique for perfusion of scala media, which is described. Injection of barium caused the endocochlear potential (EP) to increase in normal animals and had no effect on the EP of deaf, Waltzing guinea pigs. Perfusion of the ionophores caused a decline in the EP in both normal and Waltzing guinea pigs. Only the 'two-pump' model (Na/K-ATPase-mediated cation pump on the basolateral membrane and rheogenic K transporter at the luminal membrane) is consistent with the results. The cellular heterogeneity of the cochlear duct, however, introduces a measure of uncertainty into this interpretation.
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PMID:Response of cochlear potentials to presumed alterations of ionic conductance: endolymphatic perfusion of barium, valinomycin and nystatin. 631 49

Measurement of transepithelial potassium fluxes in the absence of transmural electrochemical potential gradients showed that the isolated turtle colon can actively absorb and actively secrete K+. Under short-circuit conditions the active secretory flow was inhibited by mucosal amiloride, whereas the absorptive flow was unaffected by the diuretic. The effects of ouabain and barium on secretory flow were consistent with a simple model involving basolateral uptake by an Na+-K+-ATPase and conductive exist across the apical and basolateral membranes. The active absorptive flux was blocked by mucosal ouabain and by serosal barium. The opposing active flows clearly represented cellular K+ transport, whereas paracellular K+ flows behaved as expected for a free-solution shunt.
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PMID:Potassium transport by turtle colon: active secretion and active absorption. 670 45

The nature of K-induced relaxations of the isolated rat anococcygeus muscle was studied in Tyrode's solution containing a variety of smooth muscle stimulants. When the tone of the preparation was raised by ACh (1 X 10(-6) M), the inhibitory responses to excess K (20-50 MM) were almost completely prevented by tetrodotoxin (1 X 10(-6) M) but not affected by ouabain (2 X 10(-4) M). When the preparation was contracted by barium (5 X 10(-3) M), tetraethylammonium (3 X 10(-2) M) or procaine (8 X 10(-3) M), relaxations by excess K (10-60 mM) were not affected by tetrodotoxin but completely inhibited by ouabain. It is concluded that two types of K-induced relaxations can occur depending on the smooth muscle stimulant used for elevating the tone of the preparation: the one is due to an activation of the electrogenic Na pump mediated by Na+, K+ ATPase of the smooth muscle membrane, the other is due to a stimulation of the inhibitory nerves by K.
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PMID:Potassium-induced relaxation of the rat anococcygeus muscle. 738 58

In this report, it is shown that the platelet-activating factor (PAF) induced, in human B lymphoblastoid cells, 86Rb+ influx and efflux suggesting that it activated a K+ channel. Opening of this channel was dependent on PAF-induced Ca2+ mobilization. Ionomycin and thapsigargin--a specific inhibitor of (Ca(2+)-Mg2+)-ATPase--mimicked the effect of PAF both on intracellular calcium and activation of the channel. This channel was inhibited by charybdotoxin, high doses of tetraethylammonium and barium but was insensitive to apamin, 4-aminopyridine. These features indicate that PAF activated a Ca(2+)-dependent K+ channel. In these cells, PAF also induced the expression of c-fos oncogene. This effect was not affected by charybdotoxin indicating that this channel is not involved in the control of early gene transcription.
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PMID:Platelet-activating factor activates a Ca(2+)-dependent K+ channel which is not involved in c-fos expression in human B lymphoblastoid cells. 750 33

Rabbit lenses were bathed within a bicameral Ussing-type chamber under short-circuit conditions. In this situation the short-circuit current (Isc) reflects, across the anterior aspect, the presence of anteriorly facing K+ conductance(s) plus the Na(+)-K+ pump current. Across the posterior surface the Isc is primarily carried by the movement of Na+ from the posterior bathing solution to the lens. Addition of acetylcholine (ACh) to the posterior hemichamber did not affect the translens electrical parameters; but, its introduction to the anterior bath at 1 microM immediately reduced the Isc from 8.91 +/- 1.47 to 5.84 +/- 1.28 microA cm-2 and increased the translens resistance from 1.50 +/- 0.08 to 1.59 +/- 0.09 K omega cm2 (+/- S.E.S; P < 0.05 as paired values, n = 25 lenses). The suppressed Isc gradually recovered and reached 75% of the control value 5 min after the introduction of the neurotransmitter. In six cases the recovery was nearly complete (> or = 95% of control) within this time. The preaddition of 0.1 microM atropine prevented an effect by 1 microM ACh. When atropine was added within 1 min of ACh, the suppressed Isc immediately recovered. The ACh-elicited Isc suppression was averted in lenses pre-exposed to either K+ channel blockers (quinidine or barium) or to the endoplasmic reticular Ca(2+)-ATPase inhibitor thapsigargin (Tg: 0.1 microM), which in itself produced Isc inhibitions similar to those seen with ACh under control conditions. Similarly comparable were the ACh-evoked Isc inhibitions garnered upon introduction of the agonist to lenses bathed in the absence of extracellular Ca2+. In these cases, however, the Isc recovered fully within 2-3 min. This condition also revealed that the anterior removal of medium Ca2+ increased the Isc by about 50%, a completely reversible phenomenon; Ca2+ restoration in the presence of the Ca2+ channel blocker, nifedipine (10 microM), blunted markedly the reversal to the control Isc. Overall, these results suggest that ACh receptor activation induces the release of intracellularly stored Ca2+, which in turn leads to the temporary deactivation of a K+ conductance(s); in addition, secondary Ca2+ inflow may further extend the observed inhibition. During this study, the Isc of about 30% of the lenses used spontaneously oscillated (common duration of 30 min, with a mean peak frequency of 0.76 +/- 0.32 cycle min-1 and mean amplitude of 4.07 +/- 2.65 microA cm-2; +/- S.D.S, n = 24). Experiments attempted to determine the sensitivity of the oscillatory activity to ACh. Tg, nifedipine, and the phorbol ester PMA.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Acetylcholine modulation of the short-circuit current across the rabbit lens. 755 76

Unless renal function is impaired or rhabdomyolysis is severe, hyperkalemia is a relatively uncommon metabolic complication of poisoning. In contrast, marked hypokalemia is a more common problem and may have serious sequelae. Most potassium disturbances in acute poisoning are due to disruption of extra-renal control mechanisms, notably the activity of Na+/K+ ATPase and K+ channels. Hypokalemia occurs because of increased Na+/K+ ATPase activity (e.g. beta 2 agonist, theophylline or insulin poisoning), competitive blockade of K+ channels (e.g. barium or chloroquine poisoning), gastrointestinal losses and/or alkalosis. Hyperkalemia follows inhibition of Na+/K+ ATPase activity (e.g. by digoxin), increased uptake of potassium salts, disruption of intermediary metabolism (e.g. cyanide poisoning), activation of K+ channels (e.g. fluoride poisoning), and the presence of acidosis and rhabdomyolysis, particularly if the latter is complicated by renal failure. Hypokalemia results in generalized muscle weakness, paralytic ileus, ECG changes (flat or inverted T waves, prominent U waves, ST segment depression) and cardiac arrhythmias (atrial tachycardia +/- block, AV dissociation, VT, VF). Hyperkalemia is associated with abdominal pain, diarrhea, muscle pain and weakness, ECG changes (tall peaked T waves, ST segment depression, prolonged PR interval, QRS prolongation) and cardiac arrhythmias (VT, VF). Significant disturbances of potassium homeostasis are often unrecognized and may cause considerable morbidity and mortality. Prompt recognition and appropriate treatment of these disturbances could be life-saving.
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PMID:Disturbances of potassium homeostasis in poisoning. 762 96


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