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)

Agonist occupancy of the cloned human serotonin (5-HT)1A receptor expressed in HeLa cells stimulates Na+/K+ ATPase activity as assessed by rubidium uptake. The purpose of the study was to determine which of the receptor-associated signaling mechanisms was responsible for this effect. 5-HT stimulated Na+/K+ ATPase 38% at 2 mM extracellular potassium, an effect characterized by a decrease in apparent K0.5 from 2.8 +/- 0.3 to 1.8 +/- 0.3 mM potassium without a significant change in apparent Vmax. The EC50 for the transport effect was approximately 3 microM 5-HT. The response was pertussis toxin-sensitive but did not involve inhibition of adenylate cyclase, as stimulation of Na+/K+ ATPase by 5-HT was observed in the presence of excess dibutyryl cAMP. Protein kinase C was not required for the response since short-term incubation with the phorbol esters phorbol 12 myristate, 13 acetate (PMA) and phorbol 12,13-dibutyrate (PDBu) did not mimic the 5-HT effect. Moreover, 5-HT increased Na+/K+ ATPase activity after inactivation of protein kinase C by overnight incubation with PMA. 5-HT and the sesquiterpene lactone thapsigargin increased cytosolic calcium in this cell model, and the EC50 for 5-HT corresponded with that for stimulation of Na+/K+ ATPase. Both thapsigargin and A23187, a calcium ionophore, also increased Na+/K+ ATPase activity in a dose-responsive fashion. The response to 5-HT, thapsigargin, and A23187 was blocked by conditions that removed the cytosolic calcium response. By two-dimensional gel electrophoresis, we established evidence for a calcium-sensitive but protein kinase C-independent signaling pathway. We conclude that the 5-HT1A receptor, which we have previously shown to stimulate phosphate uptake via protein kinase C, stimulates Na+/K+ ATPase via a calcium-dependent mechanism. This provides evidence for regulation of two separate transport processes by a single receptor subtype via different signaling mechanisms.
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PMID:Short-term regulation of Na+/K+ adenosine triphosphatase by recombinant human serotonin 5-HT1A receptor expressed in HeLa cells. 217 7

Advances have been made in the characterization of 5-HT-storing organelles of neurectodermal cells. The parafollicular cell of the thyroid has been used as a model. This cell stores 5-HT, shares many properties with neurons, and can be induced to change its phenotype from endocrine to neuronal by exposure in vitro to NGF. The membranes of isolated parafollicular 5-HT storage vesicles appear to contain a chloride channel that is gated in response to stimulation of the cells by secretogogues. Opening of this channel permits the interior of the vesicle to acidify in response to the action of a H+ ATPase in the vesicular membrane. Development of a delta psi appears to limit acidification of the vesicular interior when the chloride conductance is low. Transmembrane transport of 3H-5-HT into parafollicular vesicle is inhibited by dissipating the delta pH across the granular membranes. The physiological significance of the ability of parafollicular vesicles to modify the internal pH of their 5-HT-storing organelles remains to be determined. Like the synaptic vesicles of central and peripheral serotonergic neurons parafollicular vesicles contain a specific 5-HT binding protein, SBP. 5-HT storage organelles and SBP have been found in medullary thyroid carcinoma (MTC) cells, a tumor line derived from parafollicular cells. The cell biology of SBP is now under study utilizing the MTC cells.
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PMID:Serotonin-storing secretory vesicles. 225 32

Serotonin (5-HT) modulation of brain (Na+,K+)ATPase, has recently been proposed. Activation curves of the enzyme activity dependent on 5-HT concentration have previously been observed in various brain regions of normal rats. In the present study, we report the absence of 'normal' (Na+,K+)ATPase response to 5-HT in cerebral cortex, striatum and diencephalon of kindled rats.
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PMID:Serotonin-dependent (Na+,K+)ATPase in kindled rats: a study in various brain regions. 254 Aug 82

Neurotransmitter receptor binding and Na+, K+-ATPase activity were examined in the brains of six rats exposed to 7 days of microgravity during the flight of Spacelab 3. The same variables were examined in a group of six ground control rats. 5-HT1 receptor number in the hippocampus was significantly elevated by exposure to the microgravity environment, and cortical sodium-potassium pump activity was significantly depressed. A marginal depression in dopamine D-2 binding in the striatum was noted. Dopamine and 5-HT binding in a wide variety of other central regions, in addition to GABAA, muscarinic acetylcholine, adenosine A1, and opiate receptor binding, and adrenoceptor binding, was unaffected by microgravity exposure.
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PMID:Effects of microgravity on brain neurotransmitter receptors. 254 43

In a treatment regimen designed to simulate clinical situations, d-fenfluramine was administered chronically (28 days) via osmotic minipumps to lean and obese female rats. Drug effects were assessed in dietary obese, ovariectomized obese, estradiol-treated ovariectomized and unoperated Chow-fed rats. Various central and peripheral effects of d-fenfluramine were measured and compared to effects of dietary restriction as well as posttreatment changes. d-Fenfluramine suppressed food intake and body weight in all but estradiol-treated rats and was especially effective in obese ovariectomized rats. This method of administration did not deplete brain 5-HT within 28 days. The measured drug actions that may be important in: appetite suppression and weight loss include chronic stimulation of brain 5-HT activity without depletion; stimulation of (Na+- K+)ATPase activity; reduction in lipoprotein lipase activity and effects on carbohydrate metabolism.
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PMID:Long term actions of d-fenfluramine in two rat models of obesity. I Sustained reductions in body weight and adiposity without depletion of brain serotonin. 262 Oct 55

The role of the endothelium in response to aggregating platelets was examined in porcine coronary and peripheral (carotid, femoral and renal) arteries from normal and hypercholesterolemic pigs. Male Yorkshire pigs were fed either a normal diet or a 2% high cholesterol diet for 10 weeks. Endothelium-dependent responses were examined in vitro. In all arteries from control animals, aggregating platelets caused endothelium-dependent relaxations, which were augmented by ketanserin (a 5-HT2-serotonergic blocker), attenuated by apyrase (an adenosine diphosphatase and triphosphatase) or methiothepin (a combined 5-HT1 and 5-HT2-serotonergic blocker) and were almost abolished by a combination of apyrase and methiothepin. The platelet-induced relaxations were most pronounced in the coronary arteries. Adenosine diphosphate caused endothelium-dependent relaxations, which were significantly attenuated by apyrase. Serotonin also caused endothelium-dependent relaxations, which were significantly attenuated by methiothepin but augmented by ketanserin. The endothelium-dependent relaxations to adenosine diphosphate were most pronounced in coronary arteries and those to serotonin in coronary and renal arteries. In cholesterol-fed animals, the endothelium-dependent relaxations to aggregating platelets, adenosine diphosphate and serotonin were impaired in all four arteries. These experiments indicate that 1) the endothelium exerts inhibitory effects against aggregating platelets in porcine coronary and peripheral arteries; 2) platelet-induced endothelium-dependent relaxations are achieved by purinergic and 5-HT1-serotonergic receptors on the endothelium; and 3) hypercholesterolemia reduces the endothelium-dependent relaxations to aggregating platelets in a generalized manner because it impairs the relaxations to adenosine diphosphate and serotonin released from the platelets.
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PMID:Hypercholesterolemia causes generalized impairment of endothelium-dependent relaxation to aggregating platelets in porcine arteries. 278 7

A decrease in platelet 5-HT content linked to partial inhibition of 5-HT uptake has been described in essential hypertension. Transport of 5-HT through platelet membrane is dependent upon transmembranal Na+ and K+ gradients. It is inhibited by Na+, K+-ATPase inhibitors such as ouabain and endogenous digitalis-like compounds isolated from hemodiafiltrate. The activity of such compounds in plasma extracts, measured by inhibition of Na+,K+-ATPase or ouabain binding to human erythrocytes, and platelet 5-HT content were determined in parallel in essential hypertensive patients. Significant negative correlations were observed between these parameters in men, suggesting that high levels of digitalis-like compounds can affect platelet 5-HT content. In addition, in essential hypertensive patients, total plasma cholesterol was inversely related to both platelet 5-HT content (n = 15, r = -0.594, P less than 0.02) and maximal velocity of 5-HT uptake (n = 15, r = -0.717, P less than 0.003). In normotensive control subjects, no variation of platelet 5-HT content with cholesterol was observed. This suggests that the platelet membranes of essential hypertensive patients are more sensitive to increases in plasma cholesterol than those of normotensive subjects.
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PMID:Platelet 5-HT content and uptake in essential hypertension: role of endogenous digitalis-like factors and plasma cholesterol. 285 93

Hydralazine, a hypotensive agent, induces relaxation on smooth musculature. Several mechanisms related to membrane processes have been proposed to explain its relaxing action. In the present paper, the effects of hydralazine on ATPase activity in rat aorta have been studied. Hydralazine (10(-4)-5 X 10(-3) M concentration-dependently relaxed the isolated rat aortic arterial strips under norepinephrine-, serotonin- and K+-contractures. 5-Hydroxytryptamine contractures were more sensitive to the effects of hydralazine than noradrenaline- and potassium-contractures. We found that hydralazine does not modify ATPase activity on rat aorta homogenates. On the other hand, ATPase activity of rat aorta homogenates is dependent on divalent cations Ca2+ and Mg2+, and a little Na, K-ATPase activity was found.
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PMID:Hydralazine-relaxing effect on rat aorta is not mediated through changes in ATPase activity. 295 16

A spinal cord injury was produced in Wistar rats by extradural compression of the cord with a Sugita aneurysm clip for 5 seconds. During a 2-week observation period following the injury, the tissue norepinephrine (NE), dopamine (DA), and serotonin (5-HT) concentrations decreased uniformly at and below the injured site. The chemical denervation of NE or 5-HT neurons produced by the intraspinal injection of 6-hydroxydopamine (6-OHDA) or 5,7-dihydroxytryptamine (5,7-DHT) 2 weeks before the injury did not cause a marked difference in the extent of hemorrhagic necrosis of the spinal cord after trauma as compared to control animals without pretreatment. In the rats pretreated with 6-OHDA, NE was decreased to less than 30% of control (non-pretreated) values, and, beginning at 5 days after injury, motor performance (assessed quantitatively with the inclined-plane method) was significantly improved compared to results in the non-pretreated control rats. The rats pretreated with 5,7-DHT showed no change from control animals. Spinal cord samples from non-pretreated control animals obtained at the injury site 30 minutes after the compression injury showed a marked decrease in the activity of synaptosomal Na+-K+-ATPase (adenosine triphosphatase) of about 50%, and an increase in both thiobarbituric acid reaction substance (about 170%) and cyclic guanine monophosphate (about 150%). The NE-denervated rats showed no significant changes in these three parameters. The results indicated that NE released after crush injury may impair the neuronal cell membrane around the lesion site by induction of lipid peroxidation. The possible mechanisms by which released NE may alter membrane function are discussed.
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PMID:Role of monoamines in experimental spinal cord injury in rats. Relationship between Na+-K+-ATPase and lipid peroxidation. 298 70

The experiments on white rats have shown that gutimin is capable of reactivating Na, K-ATPase of the synaptosomes of the jugular spinal cord in type C botulinic intoxication. Serotonin prevented Na, K-ATPase activity inhibition only in preclinical period of intoxication. Parmidin injection did not prevent suppression of Na, K-ATPase activity either in preclinical period or in skeletal muscle paresis.
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PMID:[Possibilities of pharmacologic correction of Na, K-ATPase activity in the spinal cord in botulism]. 299 53


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