Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P20020 (adenosine triphosphatase)
 3,299 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A smooth muscle cell line (H7CM) was established from the ciliary muscle of a 1-day-old human infant. The cultured cells had a normal female karyotype (46 XX) and could be maintained in cell culture for at least 11 generations. A common feature of confluent cultures was the presence of abundant bundles of 6-7 nm microfilaments associated with dense bodies. Both the ultrastructural appearance and the presence of smooth muscle-specific alpha-isoactin (also present in the human ciliary muscle in situ) support the smooth muscle origin of the H7CM cell line. Continuous membrane voltage (Vm) recordings were obtained in confluent monolayers of H7CM cells using glass microelectrodes. Resting Vm in 105 impalements averaged -66.2 +/- 0.7 mV (mean +/- standard error of the mean). In this system, rapid membrane transients induced by changing of the superfusing test solutions were detectable. Relative K+ conductance was characterized, and the contribution of electrogenic sodium/potassium adenosine triphosphatase to Vm was investigated. Under control conditions, H7CM cells were electrically quiescent. However, action potentials could be induced by application of 10 mM barium. Barium-induced action potentials were not abolished by removal of extracellular Na+ nor were they inhibited by the presence of tetrodotoxin. However, they were blocked by verapamil, fulfilling criteria believed to be typical for smooth muscle cells. Acetylcholine, carbachol, and to a lesser extent pilocarpine induced a reversible Vm depolarization. The effect of acetylcholine was blocked by atropine, implying muscarinic receptor involvement in the Vm response. Collectively, these findings show the potential usefulness of cultured ciliary muscle cells in understanding further the cellular mechanisms underlying drug-induced contraction of the human ciliary muscle.
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PMID:Membrane voltage recordings in a cell line derived from human ciliary muscle. 217 89

Nervous or hormonal stimulation of salivary secretion in vivo is associated with a pronounced efflux of K+ from the secretory, acinar cells into the blood. This K+ efflux is followed in the post-stimulus period by a reuptake of K+ into the glandular tissue. In the present study we monitor the changes in [K+] of physiological solutions perfusing a flow chamber containing isolated segments of mouse submandibular glands. Nervous stimulation or the application of exogenous acetylcholine (ACh, 10(-5) M) to the isolated glandular tissue results in characteristic changes in the [K+] of the superfusate, indicating net K+ release followed by K+ reuptake. The post-stimulus reuptake of K+ is shown to be susceptible to blockade by either ouabain (10(-3) M) or piretanide (10(-4) M). The reuptake was markedly attenuated if Cl- in the superfusate was replaced by either NO3- or SO4(2-). The K+ uptake was, however, unaffected when Br- replaced Cl- in the superfusate. Similar effects were observed in the unstimulated glandular tissues. The introduction of Cl-(-)free media containing either NO3- or SO4(2-) resulted in a loss of K+ from the tissue which was followed, upon reintroduction of Cl-, by a pronounced uptake of K+. When Br- was substituted for Cl- there was very little change in [K+] upon removal or reintroduction of Cl-. The uptake of K+ induced by reintroduction of Cl- after a period of NO3- or SO4(2-) superfusion was blocked by both ouabain and piretanide. This uptake of K+ was also dependent on the presence of extracellular Na+. Both Cl- and Na+ had to be present in the superfusing medium for K+ uptake to be fully manifest. These findings indicate that the K+ uptake observed in both the resting and stimulated submandibular gland cannot be explained as solely due to the activity of the Na+-K+-adenosine triphosphatase (Na+-K+-ATPase). The demonstrated anionic selectivity, dependence on extracellular Na+ and susceptibility to blockade by the diuretic piretanide would strongly suggest that a coupled Na+-K+-Cl- co-transport system operates in submandibular glands as it does in other transporting epithelia to achieve K+ uptake.
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PMID:Potassium uptake in the mouse submandibular gland is dependent on chloride and sodium and abolished by piretanide. 379 14

The electrophysiological properties of embryonic chick hearts (ventricles) change during development; the largest changes occur between days 2 and 8. Resting potential (E(m)) and peak overshoot potential (+E(max)) increase, respectively, from -35 mv and +11 mv at day 2 to -70 mv and +28 mv at days 12-21. Action potential duration does not change significantly. Maximum rate of rise of the action potential (+V(max)) increases from about 20 v/sec at days 2-3 to 150 v/sec at days 18-21; + V(max) of young cells is not greatly increased by applied hyperpolarizing current pulses. In resting E(m) vs. log [K(+)](o) curves, the slope at high K(+) is lower in young hearts (e.g. 30 mv/decade) than the 50-60 mv/decade obtained in old hearts, but the extrapolated [K(+)](i) values (125-140 mM) are almost as high. Input resistance is much higher in young hearts (13 M ohm at day 2 vs. 4.5 M ohm at days 8-21), suggesting that the membrane resistivity (R(m)) is higher. The ratio of permeabilities, P(Na)/P(K), is high (about 0.2) in young hearts, due to a low P(K), and decreases during ontogeny (to about 0.05). The low K(+) conductance (g(K)) in young hearts accounts for the greater incidence of hyperpolarizing afterpotentials and pacemaker potentials, the lower sensitivity (with respect to loss of excitability) to elevation of [K(+)](o), and the higher chronaxie. Acetylcholine does not increase g(K) of young or old ventricular cells. The increase in (Na(+), K(+))-adenosine triphosphatase (ATPase) activity during development tends to compensate for the increase in g(K). +E(max) and + V(max) are dependent on [Na(+)](o) in both young and old hearts. However, the Na(+) channels in young hearts (2-4 days) are slow, tetrodotoxin (TTX)-insensitive, and activated-inactivated at lower E(m). In contrast, the Na(+) channels of cells in older hearts (> 8 days) are fast and TTX-sensitive, but they revert back to slow channels when placed in culture.
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PMID:Changes in membrane properties of chick embryonic hearts during development. 426 8

1 Secretion of catecholamines (CA) evoked by ouabain, chlormadinone acetate (CMA), phenoxybenzamine (Pbz) and vanadate, four agents known to inhibit Na(+), K(+)-dependent Mg(2+)-activated adenosine triphosphatase (ATPase) activity has been studied in suspensions of bovine isolated adrenal medullary cells.2 Acetylcholine (ACh) evoked a 5 fold increase of the basal CA secretion from isolated cells suspended in oxygenated Krebs-bicarbonate solution kept at 27 degrees C. Secretion was antagonized by Ca(2+)-deprivation or hexamethonium, indicating good functional viability of the cells.3 Ouabain (10(-7) to 10(-4) M) evoked a progressive, dose-dependent release of CA from cell suspensions. Study of the time course of the secretory response for 2 h allowed the separation of two components in the secretory response at all doses studied: a slow initial component (0.011 pg/min CA) and a second faster component (0.032 pg/min CA).4 CMA evoked a clear-cut CA secretory response. The ED(50) for CMA was 10(-4) M, as compared to 3 x 10(-6) M for ouabain. Pbz and vanadate did not induce CA release.5 [(3)H]-ouabain was taken up and bound to intact isolated cells by a non-saturable binding process. However, in semi-purified plasma membranes from bovine adrenal medulla a saturable specific [(3)H]-ouabain binding process was observed with a K(D) of 8.1 nM. Binding to the membranes was ATP-dependent and antagonized by K(+).6 [(3)H]-ouabain specific binding to membranes was antagonized by ouabain and CMA, but not by Pbz or vanadate; the ID(50) for ouabain and CMA were 10(-6) and 10(-5) M respectively.7 Ouabain partially inhibited, in a dose-dependent manner, Na(+), K(+)-Mg(2+) ATPase activity of the semi-purified plasma membranes.8 The results demonstrate a good correlation between the ability of different drugs, known to inhibit ATPase activity, to displace [(3)H]-ouabain binding to adreno-medullary plasma membranes and their capacity to evoke a CA secretory response from isolated chromaffin cells. The data also suggest that the CA secretory effects of ouabain may not be due simply to inhibition of the Na(+) pump and the subsequent ionic redistribution across the plasma membrane; a second mechanism may also be involved.
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PMID:Correlation between catecholamine secretion from bovine isolated chromaffin cells and [3H]-ouabain binding to plasma membranes. 616 27

The present experiment was conducted to establish the relationship between selected physiological parameters and histological responses of Channa punctatus brain tissue to endosulfan exposure. The fish (35.6 +/- 0.7 g) was exposed to sublethal endosulfan concentration (8.1 microg l(-1)) for a period of 12, 24, 36, 48, 72, and 96 h. Results showed that brain glucose level increased significantly after exposure, indicating a hyperglycemic state of the fish. Brain vitamin C level decreased with an increase in the exposure time. Acetylcholine esterase and adenosine triphosphatase enzyme activities also showed a significant reduction upon endosulfan exposure. Brain histopathology after 96 h endosulfan exposure showed that the apical lobe of the cerebrum (the only portion examined) had mild necrosis. Focal area of gliosis could be seen in the cerebrum, which were absent in the control fish. The results indicate that exposure of sublethal concentration of endosulfan to C. punctatus may have a direct effect on the histology of the fish's brain tissue, thereby affecting its metabolism.
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PMID:Biochemical and histological changes in the brain tissue of spotted murrel, Channa punctatus (Bloch), exposed to endosulfan. 1952 21