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)

Microsomal preparations of Na, K-ATPase, isolated from dog and bovine brains, were completely insensitive to acetylcholine (10(-6)-10(-2) M) under standard experimental conditions. At the same time, heat pretreatment of membranes induced alterations of the enzymatic activity in presence of low concentrations (10(-6)-10(-5) M) of the neurotransmitter. Acetylcholine stimulated the Na, K-ATPase activity after storage of the preparations at 22 degrees within 30 or 60 min inhibited the activity at 37 degrees. Addition of the transmitter during the preincubation increased its effect. The maximal values of Na, K-ATPase activation and inhibition constituted 30% and 24%, respectively. D-tubocurarine (10(-6)-10(-5) M) and atropine (10(-4) M) did not eliminate and eserine (10(-4) M) did not alter the induced effect of acetylcholine. The effects of acetylcholine were changed to the opposite ones within 70-90 days of storage of the preparations. The phenomenon might be simulated by "ageing" of microsomes at 37 degrees within 3-6 hrs.
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PMID:[Sensitivity of brain Na, K-ATPase to acetylcholine following heat treatment of membrane preparations]. 625 67

[3H]Acetylcholine efflux and Na+-K+ ATPase ion pump activity were measured concomitantly in rat cortical synaptosomes. Ouabain (500 microM), strophanthidin (500 microM), and parachloromercuribenzene sulfonate (500 microM) each inhibited ouabain-sensitive 86Rb uptake and elevated [3H]acetylcholine release independently of the external calcium concentration. Veratridine (10 microM), electrical field stimulation (60 V, 60 Hz, 5-ms pulse duration), or the calcium ionophore A23187 (10 micrograms/ml) also inhibited ouabain-sensitive 86Rb uptake and released [3H]acetylcholine, but via a calcium-dependent process. Veratridine-induced [3H]acetylcholine release and ion pump inhibition were correlated over a wide range of drug concentrations and both effects were blocked by pre-treatment with tetrodotoxin (1 microM). The rate of [3H]acetylcholine efflux from superfused synaptosomes was increased within 15 s of exposure to ouabain, strophanthidin, veratridine, A23187, or field stimulation, while ouabain-sensitive 86Rb uptake was significantly decreased within a similar interval. These results suggest that [3H]acetylcholine release is due at least in part to inhibition of Na+-K+ ATPase.
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PMID:Correlations between Na+-K+ ATPase activity and acetylcholine release in rat cortical synaptosomes. 625 54

The effect of vanadate (0.5 mumol/min) on renin secretory rate (RSR) of the kidney has been studied in nembutal-anesthetized, volume-expanded dogs. Intrarenal vanadate infusion caused a 69.3 +/- 8.8% decrease in RSR. This was accompanied by marked decreases in renal blood flow (RBF), glomerular filtration rate (GFR) and fractional excretion of sodium (FENa). Renal vascular resistance rose from 1.3 +/- 0.09 to 6.1 +/- 2.3 mm Hg/ml/min (P less than .0005). Papaverine infusion partially blunted the effect of vanadate on RSR (RSR only fell to 42. +/- 10% of basal values). The decreases in RBF and GFR were also less and FENa slightly higher than normal. Acetylcholine prevented the effects of vanadate more fully. There was no fall in RBF, GFR or FENa and it basically abolished the fall in RSR which fell only 19.4 +/- 25.3 of control (P = N.S.). Nifedipine (a slow Ca++ channels blocker) also prevented the fall in RBF, GFR and FENa induced by vanadate. RSR did not change significantly (7.8 +/- 10.9%). These results clearly demonstrate that vanadate is a potent inhibitor of renin secretion and suggest that inhibition of smooth muscle Na+, K+, adenasine triphosphatase and changes in the cystosolic concentration of Na and Ca are involved in its mechanism. Changes in perfusion pressure and sodium delivery to the macula densa appear to have little if any role in the inhibition.
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PMID:Effect of sodium orthovanadate on renal renin secretion in vivo. 628 12

Preincubation of rat brain homogenates with acetylcholine (ACh) in concentrations of 10(-3)-10(-5) M for 60 minutes produces an essential increment (15-30%) in activity of microsomal Na, K-ATPase. Analogous effect was exerted by the acetylcholinesterase inhibitor eserine (10(-5)-10(-6) M). Acetylcholine has no effect in the presence of actinomycin D. Dialysis of microsomes isolated from the homogenate incubated with ACh leads to a decrease in the enzyme activity and release to the dialysate of low-molecular factor activating Na, K-ATPase of intact microsomes. The latter fact evidences the ACh-induced synthesis of activating factor and inhibition of Na, K-ATPase synthesis. After the animals are administered eserine (0.2-0.4 mg/kg), isolated microsomes show a reduced level of Na, K-ATPase (by 10-15%). Dialysis of microsomes leads to an appreciable elevation (by approximately 40%) of the enzyme activity and release into the dialysate of the inhibitory factor. The differences in the effects of eserine in vivo and in vitro suggest that during the impairment of brain integrity certain effects are excluded from the processes of the control over Na, K-ATPase activity. One of these may involve the impairment of intercellular interactions, for example, the disappearance of the effect on cholinoceptive cells of internuncial neurons that release inhibitory neurotransmitters (catecholamines).
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PMID:[Endogenous activators and inhibitors of Na, K-ATPase induced by acetylcholine]. 629 34

The dependency of fluid secretion on extracellular Na+ and the levels of phosphorus compounds were studied in the perfused canine mandibular gland (using 31P-NMR). During control perfusion, the resting levels of creatine phosphate (CP) and ATP were 0.62 +/- 0.05 mmol . kg-1 gland and 0.42 +/- 0.04 mmol . kg-1 (mean +/- S.E., n = 9), respectively. Acetylcholine (Ach; 1 mumol . l-1 for 3 min) induced a salivary secretion and decreased the CP level. When Na+ in the perfusate was completely replaced with Li+, Ach induced only a minimal salivary secretion and no change in the ATP and CP levels. Restitution of Na+ to the perfusion, even without added Ach, caused a decrease in ATP and CP, and a small increase in salivary secretion. These results suggest that the activity of Na+/K+ ATPase is increased inversely via a rise of the intracellular Na+ concentration and that the salivary secretion is induced not only by added secretagogues but by an increase in the Na+ entry without added secretagogues.
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PMID:Effects of Na+ depletion on fluid secretion and levels of phosphorus compounds as measured by 31P-NMR in perfused canine mandibular gland. 650 28

Male rats fed on pellet diet to an average weight of 105 g were placed on a vitamin E deficient diet containing 20% coconut oil for a period of 12 weeks at two dietary protein levels, 20% and 10% casein. Rats on 20% casein diet showed a definite weight loss but not so at the 10% casein level. A marked increase in the liver in vitro lipid peroxidation was observed at both protein levels. Feeding of retinyl palmitate at 100,000 IU/100 g body weight for 4 consecutive days inhibited the liver, brain and kidney in vitro peroxidation; megadoses of ascorbic acid produced less inhibition of the liver peroxidation, but the same degree of inhibition for brain and kidney peroxidation as in vitamin A loaded rats. Both dietary palmitate or ascorbic acid. Acetylcholine esterase and ATPase, two of the membrane enzymes of erythrocytes, were depressed in all the groups. The glutathione content of erythrocytes was increased in rats given ascorbic acid. In all the groups the higher dietary protein levels produced greater loss of body and tissue weights. It is concluded vitamin E deficient diet supplemented with dietary coconut oil (saturated fat) induces increased in vitro lipid peroxidation and oxidative lysis of erythrocytes and that megadoses of vitamin A or C suppress the in vitro lipid peroxidation but enhance the lysis.
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PMID:Effect of dietary coconut oil and casein and megadoses of vitamin A or C on tissue lipid peroxidation and hemolysis in vitamin E deficiency. 665 Mar 2

The chick wrist muscle ulnimetacarpalis dorsalis (umd) has two heads. Using myosin ATPase and acetylcholinesterase (ACh.E) staining it was shown that one of the heads is composed almost entirely of acid-stable muscle fibres with multiple end plates (slow muscle fibres) and the other of acid-labile fibres with single end plates (fast muscle fibres). The development of the muscle was traced from E7 (Stage 32-33) when it is a relatively homogeneous mass, to E18. The two heads of the muscle are first distinguishable, by ATPase staining, at E8 (Stage 33-34) prior to their cleaving. Both heads of the muscle are innervated by motoneurons positioned laterally in the lateral motor column in spinal segments 15 and 16. There is no observable difference in the positions of the motoneuron pools to the two heads. At E18 the motoneurons innervating the fast head tend to be slightly larger than those innervating the slow head.
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PMID:Development and motor innervation of a distal pair of fast and slow wing muscles in the chick embryo. 666 33

Acetylcholine (ACh)-evoked flow from the main excretory duct as well as ACh-induced secretory and resting membrane potentials from cells of the rabbit lacrimal gland were recorded during perfusion with inhibitors. During perfusion with 2,4-dinitrophenol (DNP), ouabain, or ethacrynic acid, ACh-induced flow was 5%, 20%, and 8% of control, respectively; ACh-induced hyperpolarizing secretory potential was 64%, 50%, and 63% of control, respectively; and the resting membrane potential was 79%, 64%, and 73% of control, respectively. Only during perfusion with ethacrynic acid was there a significant increase in the number of cells that did not respond to ACh with a change in potential. We have concluded that (1) ACh-induced secretion is highly dependent on oxidative metabolism and Na-K ATPase; (2) ACh-induced hyperpolarization is dependent on changes in ionic permeabilities, Na-K ATPase, and to lesser extent oxidative metabolism; and (3) the resting membrane potential is much less dependent on oxidative metabolism and Na-K ATPase activity.
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PMID:Lacrimal gland flow and potentials during dinitrophenol, ouabain, and ethacrynic acid perfusion. 721 69

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

The molecular mechanisms responsible for the regulation of ciliary beating frequency (CBF) are only partially characterized. To determine whether elevation of intracellular Ca2+ ([Ca2+]i) can cause an increase in CBF, we measured CBF and Ca2+ in single cells. Ovine tracheal epithelial cells, obtained by dissociation with protease, were grown in primary culture for 1 to 28 days in a mucus-free system. CBF of a single cilium was measured by digital video phase-contrast microscopy and on-line Fourier-transform analysis. Changes in [Ca2+]i from single cells were determined with fura-2, using ratio imaging video microscopy. Activation of a muscarinic pathway with 10 microM ACh (acetylcholine) increased [Ca2+]i from 53 +/- 9 nM (mean +/- s.e.m.) to 146 +/- 12 nM or to 264 +/- 51% above initial baseline. In the same cells, ACh increased CBF from a baseline of 7 +/- 0.5 Hz to 9 +/- 0.2 Hz or to 31 +/- 2.8% above baseline (n = 14). The elevations of both [Ca2+]i and CBF were transient and relaxed back to an elevated plateau (10/14 cells) as long as ACh was present. To elevate [Ca2+]i by mechanisms independent of a G-protein-coupled receptor, we measured [Ca2+]i and CBF of the same cells in extracellular solutions with either 0 Ca2+ (+ 1 mM EGTA) or 10 mM Ca2+. Both signals rose and fell with similar kinetics in response to changing [Ca2+]0, suggesting that changes in [Ca2+]i alone can modulate CBF. In a second independent manipulation, cells were treated with 1 microM thapsigargin, an irreversible inhibitor of the endoplasmic reticulum Ca(2+)-ATPase. Upon thapsigargin addition, 37 of 42 cells showed a transient [Ca2+]i increase and, as measured in different experiments, 8 of 9 cells showed a transient increase in CBF. Interestingly, application of ACh after cells were treated with thapsigargin produced decreases in both [Ca2+]i and CBF in 8/8 cells. Lastly, after 1-3 days in culture, addition of 10 microM ACh often produced [Ca2+]i oscillations rather than transients in [Ca2+]i. Measurements of CBF in these cells showed frequency modulation of CBF with the same peak-to-peak time interval as the Ca2+ oscillation. These results show that: (1) CBF can be measured from a single cilium and monitored on-line to track changes; (2) CBF and [Ca2+]i can be measured in the same single cell; (3) transient changes in [Ca2+]i (induced by 4 different manipulations) are associated with kinetically similar changes in CBF; and (4) [Ca2+]i oscillations are coupled to frequency modulation of ciliary beating.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Coupling of [Ca2+]i and ciliary beating in cultured tracheal epithelial cells. 776 91


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