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)

The kinetics of K+ release from an in vitro system of rat submaxillary gland slices were studied after stimulation with parasympathomimetic secretagogues. The slices were incubated at 37degreesC in an oxygenated, enriched Krebs-Ringer bicarbonate medium in the presence and in the absence of Ca++ and of ouabain and, in some experiments, in the presence of the specific antagonists atropine (5 x 10(-6) and 2 x 10(-5) M), phentolamine (2 x 10(-5) M) or propranolol (2 x 10(-5) M. K+ release was elicited by the addition of acetylcholine (2 x 10(-5) M), pilocarpine (2 x 10(-5) M) and carbamylcholine (10(-9) to 2 x 10(-5) M). The results demonstrate that: 1) The selective stimulation of cholinergic receptors induces a rapid net release of K+ from the slices. After 10 minutes of incubation, the percent K+ released after a 2 x 10(-5) M dose of each of the three secretagogues was, respectively, 20.8%, 15.5%, and 19%. 2) The response to carbamylcholine does not occur when Ca++ is absent from the medium and is blocked by atropine but not by phentolamine or by propranolol. Atropine (5 x 10(-6) M) causes a 17-fold shift to the right on the dose-response curve to carbamylcholine. 3) The magnitude of K+ release is the ratio of two opposing mechanisms, a passive efflux and an active reuptake. The latter depends on the activity of the ouabain-sensitive Na+-K+-adenosine triphosphatase. 4) The sensitivity of the slice system to carbamylcholine seems to be greater than that to norepinephrine in terms of net K+ release after equimolar doses of 2 x 10(-5) M and also in terms of the dose required to induce a half maximal passive K+ efflux. However, the maximal passive K+ efflux is similar after both types of secretagogue and amounts of approximately 45% of the K+ present in the slices.
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PMID:Potassium release from the rat submaxillary gland in vitro. II. Induction by parasympathomimetic secretagogues. 13 10

Many plants are recommended in traditional medicine as active against various effects of snakebite. Few attempts have been made to investigate the veracity of these assertions in controlled experiments. Several workers, mainly Oriental, have investigated the reputation of such plants by performing in vitro and in vivo experiments in order to demonstrate whether there was any protective effect, using drugs or mixtures of drugs prepared using traditional formulae. In some studies, these extracts were administered to mice before or after treatment with different elapid or crotalid venoms. Other papers deal with selected compounds isolated from Schumanniophyton magnificum, Eclipta prostrata or Aristolochia shimadai, and their capacity to inhibit phospholipase A2 or other enzymes (e.g. ATPase) or for physiological and biochemical properties (such as effects on uterine tone or the protection of mitochondrial membranes). Japanese workers have described the antihaemorrhagic effect of persimmon tannin from Diospyros kaki. Atropine has been attributed a life-prolonging effect after black mamba venom treatment. Prolonged survival was also observed after pretreatment with extracts of Diodia scandens and Andrographis paniculata. Some authors have found little or no beneficial effects. The papers collected so far show that there are no systematic investigations in this field.
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PMID:Plants with a reputation against snakebite. 144 Jun 20

In guinea-pig ileal longitudinal smooth muscle, both palytoxin (PTX) and carbachol (CCh) increased K+ efflux with an EC50 of 1.8 X 10(-10) M and 4.1 X 10(-7) M, respectively. Atropine (10(-6) M) did not inhibit the K+ efflux due to PTX (3 X 10(-9) M), but completely inhibited the efflux due to CCh (10(-5) M). External Ca2+ removal and verapamil (10(-5) M) did not change the PTX-induced K+ efflux, although the CCh-induced K+ efflux was inhibited about 77% and 71%, respectively. PTX-induced K+ efflux was reduced to 31% by a depletion of intracellular Ca2+. Tetraethylammonium (15 mM) inhibited the K+ efflux due to PTX or CCh to 61% or 75%, respectively. The PTX-induced K+ efflux was also inhibited by cymarin (3 X 10(-8) M), ouabain (10(-5) M) and digitoxin (10(-5) M). These results suggest that the PTX-induced K+ efflux is less dependent on Ca2+ influx than that due to CCh. Furthermore, the binding sites for PTX in the ileal muscle of guinea-pig may be Na+, K+-ATPase, as has been suggested in other types of cells.
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PMID:Palytoxin-induced K+ efflux from ileal longitudinal smooth muscle of the guinea-pig. 289 32

Preparations of lysed synaptosomes exhibit a high affinity Ca2+/Mg2+ ATPase and ATP-dependent Ca2+ accumulation activity, with a Km for Ca2+ congruent to 0.5 microM, close to the cytosolic concentration of Ca2+. When these membrane suspensions were incubated with cholinergic agonists muscarine or oxotremorine (1-20 microM), both Ca2+/Mg2+ ATPase and ATP-dependent CA2+ uptake were inhibited in a concentration-dependent fashion. Atropine alone (0.5-1.0 microM) had no effect on either enzyme or uptake activity, but significantly inhibited the actions of both muscarine and oxotremorine. No significant effects by cholinergic agonists or antagonists were seen on fast or slow phase voltage-dependent Ca2+ channels or Na+-Ca2+ exchange. These results suggest that activation of presynaptic muscarinic receptors produce inhibition of two processes required for the buffering of optimal free Ca2+ by the nerve terminal. Activation of presynaptic muscarinic receptors have been reported to reduce the release of ACh from nerve terminals. Alterations in intracellular free Ca2+ may contribute to a reduction in transmitter (ACh) release seen following activation of cholinergic receptors.
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PMID:Activation of central muscarinic receptors inhibit Ca2+/Mg2+ ATPase and ATP-dependent Ca2+ transport in synaptic membranes. 315 60

The membrane-bound ATP-dependent energy systems (ATP-membrane ATPase-ADP and ATP-adenylate cyclase-cAMP) play an essential role in the physiological regulation of the gastrointestinal mucosa and its damage in rat and man. A good, physiologically, hormonally and pharmacologically well controlled and regulated feedback system exists between the two energy systems. The significant increase of ATP transformation into ADP or cAMP represents a causative metabolic background of the development of gastric, duodenal and jejunal ulcer (damage) in man and rat. The ulcer preventive effects of vitamin A, beta-carotene, atropine, cimetidine, prostacyclin I2, and surgical vagotomy were studied in connection with their effects on the membrane-bound ATP-dependent energy systems of the gastric, duodenal and jejunal mucosa in man and rat. Atropine and cimetidine were applied in cytoprotective and antisecretory doses, and the tissue levels of ATP, ADP, AMP, cAMP and lactate were measured. The results indicated that the disturbed equilibrium between the two energy supply systems can be modified (normalized) by drugs and surgical vagotomy; the drug effect depends on the actual biochemism of the gastroduodenal mucosa; the values of affinities (pD2) and intrinsic activities (alpha) of the different drugs differ in relation to membrane-bound ATP-splitting enzymes; the changes in the membrane-bound ATP-dependent energy systems of the damaged rat gastric mucosa, produced by vitamin A and beta-carotene, depend on their cytoprotective doses which are connected with their cytoprotective effects; the biochemical changes induced by drugs (given in cytoprotective and anti-secretory doses) differ only quantitatively but not qualitatively; the drug effects on the membrane-located ATP-splitting enzymes (membrane ATPase and adenylate cyclase) in human gastric, duodenal and jejunal mucosa are similar to those in rats, but their affinities (pD2) and also their intrinsic activities (alpha) differ to the enzyme systems.
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PMID:Molecular biochemistry and pharmacology of peptic ulcer treatment. A review. 331 63

Gastric ulcerations induced in rats by a combination of indomethacin and cold-stress (5 +/- 1 degrees C) for 6 hr were more severe than those induced by indomethacin or cold-stress alone. The acidity of gastric juice was increased in rats treated with indomethacin plus cold-stressed. Histamine H2 receptor antagonists, (H+-K+) ATPase inhibitors and prostaglandins inhibited gastric ulcer formation in indomethacin plus cold-stress treated rats, whereas anticholinergics aggravated the ulceration. The indomethacin plus cold-stress induced acid secretion was inhibited by cimetidine and omeprazole in pylorus-ligated rats. Atropine had less effect on the increase in acidity than cimetidine and omeprazole. These findings indicate that the ulcer formation in indomethacin plus cold-stress treated rats is related the increased in acidity of gastric juice. This gastric ulcer model may be useful for evaluating antiulcer agents.
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PMID:Effects of indomethacin and cold-stress on gastric acid secretion and ulceration. The effects of anti-acid secretory agents in rats. 367 83

The ability of digoxin and a 4-aminocardenolide, ASI-222, to alter atrioventricular nodal refractory period (AVRP) was determined as a function of the maximum subarrhythmic dose (MSAD) in the dog anesthetized with morphine-pentobarbital. ASI-222, a highly polar and potent inhibitor of Na+, K+-adenosine triphosphatase produces a cardiotoxicity in dogs prominently involving atrioventricular nodal blockade rather than ventricular premature ectopic beats and tachycardia seen with digoxin. AVRP was assessed with trains of electrically isolated stimuli of decreasing pulse interval delivered to the right atria. Digoxin and ASI-222 were infused i.v. at rates which produced cardiac arrhythmias in about 100 min in dogs either: 1) with intact nerves, 2) pretreated with atropine, 3) without reflex receptors (without vagus and carotid sinus nerves, 4) without cardiac sympathetic nerves and adrenals or 5) pretreated with metoprolol. In dogs with intact nerves, ASI-222 produced greater increases in AVRP than digoxin at fractions of the MSAD; however, both glycoside produced a similar elevation at the MSAD (approximately equal to 30% increase). Atropine did not alter the AVRP response to ASI-222 but prevented the lengthening due to digoxin except for that which occurred near the MSAD. Removal of reflex receptor afferents (and vagi) had an effect similar to atropine on the AVRP response to digoxin, but completely prevented any response to ASI-222. Prior sympathectomy or beta adrenergic blockade abolished the AVRP response to ASI-222 but did not alter the responses to digoxin.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of an aminocardenolide and digoxin upon atrioventricular refractory period in the dog. 407 25

Acetylcholine (ACH) produced specific inhibition of Na, K-ATP-ase activity in sarcolemmic preparations of the frog heart (K0.5 = 1 microM), dog atria (K0,5 = 5 microM) and ventricles (K0.5 = 1 microM), and dog small intestinal smooth muscles (K0,5 = 0.5 microM). K0.5 is the concentration causing a half-maximal effect. Atropine (10(-7) = 10(-6) M) blocked the inhibitory effect of ACH. The preparations contained a considerable number of 3H-quinuclidinyl benzilate (3H-QNB) binding sites. Treatment of atrial sarcolemma with a mixture of digitonin and sodium cholate resulted in a substantial decrease in the number of 3H-QNB binding sites in the membrane, while Na,K-ATPase lost responsiveness to ACH. In the presence of 10 microM GTP there was a noticeable decrease in sensitivity of the enzyme to ACH. It is assumed that inhibition of Na, K-ATPase activity by acetylcholine is mediated by muscarinic receptor activation with the involvement in this process of GTP-binding proteins.
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PMID:[M-cholinoreceptor-mediated inhibition of Na, K-ATPase activity in the myocardial sarcolemma and intestinal smooth muscles by acetylcholine]. 609 7

Dose-dependent inhibition of Na+, K+-ATPase by acetylcholine was found in dog heart sarcolemma obtained after treatment with NaI. The enzyme was completely inhibited at 1 X 10(-2) M concentration of acetylcholine (Ki = 14 +/- 2 mM). Low concentrations of acetylcholine (1 X 10(-6)--1 X 10(-5) M) increased the Na+, K+-ATPase activity, the intermediate (5 X 10(-5)--5 X 10(-4) M) and high (1 X 10(-3)--1 X 10(-2) M) concentrations decreased the activity in the preparations enriched with sarcoplasmic vesicles. Sodium dodecylsulfate enhanced the activating effect but did not affect the inhibition. Atropine (1 X 10(-6)--1 X 10(-4) M) decreased the Na+, K+-ATPase activity and protected the enzyme against the inhibitory effect of acetylcholine. The data obtained suggest that interaction of acetylcholine with integral membrane proteins (Na+, K+-ATPase and/or muscarinic acetylcholine receptors) is apparently responsible for the neurotransmitter inhibitory effect.
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PMID:[Effect of acetylcholine on the Na+,K+-ATPase activity of different preparations of myocardial sarcolemma]. 630 Nov 55

1. The effect of Na+,K(+)-ATPase inhibition by ouabain on gastric acid secretion was studied in the mouse isolated whole stomach preparation. 2. Ouabain caused a transient enhancement of histamine-induced gastric acid secretion followed by an inhibitory phase. On the other hand, ouabain caused a rapid reduction of bethanechol-stimulated acid secretion without an enhancement phase. 3. In dibutyryl cyclic AMP-induced acid secretion, ouabain led to a transient increase in acid secretion followed by a fall, as was seen with the histamine stimulation. Ouabain caused a rapid reduction of A23187-induced acid secretion. 4. Ouabain by itself increased basal acid secretion, and thereafter slowly suppressed the acid secretion. 5. Atropine inhibited both the ouabain-induced enhancement of the stimulated gastric acid secretion and the ouabain-induced stimulation of basal acid secretion. 6. The present study showed that Na+,K(+)-ATPase inhibition by ouabain caused a phasic enhancement of the stimulated gastric acid secretion through release of endogenous acetylcholine when the secretagogues act via an intracellular cyclic AMP pathway. It also inhibited the stimulated acid secretion irrespective of secretagogues, probably through its inhibitory effect on Na+,K(+)-ATPase in the gastric parietal cell.
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PMID:Differential effects of Na+, K(+)-ATPase inhibition by ouabain on acid secretory responses to histamine and bethanechol in the mouse isolated stomach. 803 67


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