Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.6.1.3 (ATPase)
 65,361 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of 5-hydroxytryptamine (5HT) on the ATPase activity and sulphydryl group reactivity of mammalian skeletal muscle actomyosin has been studied. 5HT inhibited the Mg2+-activated but not the Ca2+-activated ATPase activity of actomyosin. It slightly activated myosin ATPase. The sulphydryl groups of actomyosin reacting with 5,5'-dithiobis-(2-nitrobenzoic acid) were blocked by concentrations of 5HT which inhibited the Mg2+-activated ATPase. The significance of the results are discussed in relation to the muscle lesions in the experimental myopathy induced by 5HT and imipramine.
 ...
PMID:Inhibition of actomyosin ATPase by high concentrations of 5-hydroxytryptamine. Possible basis of lesion in 5HT-induced experimental myopathy. 13 9

The effects of iontophoretically applied Na+-, K+-dependent adenosinetriphosphatase (Na+,K+-ATPase) (EC 3.6.1.3) inhibitors (ouabain, digitoxin, digitoxigenin, strophanthin K, strophanthidin, thevetin A and B, ethacrynate, and harmaline) on the depression of rat cerebral cortical neurones by noradrenaline, 5-hydroxytryptamine, and histamine have been studied. The inhibitors antagonized depressions of spontaneously active neurones evoked by these amines, but not those evoked by gamma-aminobutyric acid, adenosine, adenosine 5'-monophosphate, or calcium. The antagonistic potencies of the various inhibitors appeared to be proportional to their known potencies as inhibitors of Na+, K+-ATPase. The data therefore support the hypothesis that amines depress central neurones by activating an electrogenic sodium pump.
 ...
PMID:Antagonism of biogenic amine-induced depression of cerebral cortical neurones by Na+, K+-ATPase in inhibitors. 14 20

The amines noradrenaline, dopamine, 5-hydroxytryptamine, and histamine (0.01-0.5 mM) enhanced the activity of Na-K-ATPase (EC 3.6.1.3) in rat cerebral cortical synaptosomal fractions. The activities of Mg-ATPase and Ca-Mg-ATPase were not significantly affected. No stimulation of Na-K-ATPase occurred in the presence of chelating agents (0.5 mM EGTA or EDTA) unless 0.5 mM calcium had also been added to the incubation medium. These results are consistent with the hypothesis that amines depress cerebral cortical neurones by activation of an electrogenic sodium pump. Calcium ions appear to be involved in this process.
 ...
PMID:Stimulation of cerebral cortical synaptosomal Na-K-ATPase by biogenic amines. 14 37

The main role in determination of the pharmacologic effects of the imipramine groups antidepressants is given to their influence on neurotransmitters metabolism in synapses, the activity of enzymic systems regulating the transport of ions, as well as on the system of cyclic AMP metabolism. Interaction of tricyclic antidepressants with membrane and, as the result, distrubance in reuptake of transmitters (epinephrine and 5-hydroxytryptamine) in neurons is supposed to be one of the mechanisms of synaptic transmission regulation. The possible role in inhibition of biological amines deamination, in particular of phenylethylamine, in antidepressive effect of tricyclic antidepressants is discussed. It is supposed that the thymoanaleptic effects of the imipramine group antidepressants are due to activation of central serotoninergic processes, and their psychoanaleptic effect due to activation of the adrenergic system. Inhibition of the Na+, K+-ATPase activity quilizing effect of tricyclic antidepressants.
 ...
PMID:[Neurochemical mechanisms of the action of tricyclic antidepressants of the imipramine group]. 19 70

Na,K-ATPase activity in glial membranes is rather low that in the nerve ending membranes, but is characterized by the same kind of Na+/K+-dependence. Glial Na,K-ATPase is insensitive to acetylcholine (ACh), 5-hydroxytryptamine (5-HT) and gamma-aminobutyric acid (GABA) while norepinephrine activates Na,K-ATPase at low concentrations and inhibits it at high concentrations. Participation of Na,K-ATPase in the regulatory mechanisms of the neuron-neuroglia relations is discussed.
 ...
PMID:[Some properties of glial membrane Na, K-ATPase]. 21 27

Synaptosomes isolated from rat brain cortex incorporated [14C]5-hydroxytryptamine at 37 degrees C with high affinity. An apparent transport constant of Kt = 50nM was found. The high affinity uptake was decreased by treatment of synaptosomes with neuraminidase from Vibrio cholerae or Clostridium perfringens prior to incubation with [14C]5-hydroxytryptamine. The inhibition was related to the amount of sialic acid released, with a Ki value of 3.5 micrometer. A non-competitive type of inhibition was observed after treatment with neuraminidase. The inhibition caused by ouabain could not be enhanced by simultaneous treatment with neuraminidase. Neuraminidase did not lower the activity of (Na + K)-ATPase or Mg2-ATPase. These results suggest that sialic acid is involved in the 5-hydroxytryptamine uptake mechanism without functional linkage to the energy pump of the membrane, which maintains the sodium gradient necessary for 5-hydroxytryptamine transport.
 ...
PMID:On the significance of sialic acid in high affinity 5-hydroxytryptamine uptake by synaptosomes. 64 May 86

Long-term (10 days) administration of imipramine [20 mg/(kg X d)] to rabbits significantly increases the Km value (4.0 micron) of 5-hydroxytryptamine uptake in their platelets compared to those of saline- (0.7 micron) or haloperidol- (0.4 micron) treated rabbits. Administration of haloperidol inhibits the 5-hydroxytryptamine uptake non-competitively, and in vitro it had an ID50 value of 22 micron. Intravenous injections of [14C]5-hydroxytryptamine were given to the animals 1 h before blood collection. After isolation of platelets, their sonicates were subjected to 30-60% continuous sucrose gradient centrifugation. The subcellular distribution of [14C]5-hydroxytryptamine indicates that imipramine treatment, in contrast to the control and haloperidol treatment, led to a shift in the exogenous 5-hydroxytryptamine peak from within the granular zone (d 1.18) to the extragranular cytoplasm (d 1.15). Compared to control values, the imipramine treatment caused 63% inhibition in the platelet Na-K-ATPase activity.
 ...
PMID:Subcellular distribution of [14C]5-hydroxytryptamine in the blood platelets of rabbits: effects of imipramine and and haloperidol. 68 Jun 41

The hormone serotonin (5-hydroxytryptamine) has been implicated as the cause of the diarrhea seen in many patients with the carcinoid syndrome. To determine whether serotonin is an intestinal secretagogue, the effect of serotonin on intestinal water and electrolyte transport was evaluated in the rabbit. Two weeks of daily subcutaneous injection of serotonin suspended in oil resulted in a blood serotonin level elevated to twice that of controls. Intestinal transport was studied in vivo by a perfusion technique. Serotonin treatment resulted in ileal secretion and decreased mid-jejunal absorption of water and electrolytes but did not effect water absorption in the proximal jejunum or colon. Intestinal absorption of D-glucose and the amino acid L-tryptophan and glucose-dependent water and electrolyte absorption were normal in serotonin-treated animals. Serotonin-induced ileal secretion was reversed by methysergide, a peripheral antagonist of serotonin action. No alterations in intestinal histology or permeability occurred in serotonin-treated animals. Serotonin-induced intestinal secretion was not associated with alterations in the activities of intestinal mucosal adenylate cyclase, cyclic nucleotide phosphodiesterase, or Na-K-ATPase.
 ...
PMID:Effect of serotonin treatment on intestinal transport in the rabbit. 83 7

The aim of the present study was to determine the influence of the sodium pump on the responses elicited by 5-hydroxytryptamine (5-HT) in segments of human placental veins. 5-HT (10(-9)-3 x 10(-7) M) elicited potent concentration-dependent vasoconstrictor responses, but a fall in tone was observed at higher concentrations. In the presence of 10(-7) M ouabain, this fall in tension was abolished. A single concentration of 5-HT (10(-6) M) produced a biphasic response, consisting in a fast early contraction followed by a slow relaxation. This relaxant phase was concentration dependently inhibited by ouabain (10(-7) and 10(-6) M), and abolished by preincubating the vessels in a K(+)-free solution and reducing bath temperature to 28 degrees C, methods usually employed to inhibit the sodium pump. After adding 7.5 mM K+ or returning the temperature to 37 degrees C, marked relaxation was observed. On the other hand, the relaxant phase with the amine remained unchanged by pretreatment with phenidone, oxyhemoglobin, indomethacin (all at 10(-5) M) and endothelium removal. 5-HT (10(-7) and 10(-6) M) elicited increases in ouabain-sensitive 86Rb+ uptake. These results suggest that: (1) 5-HT activates Na+,K(+)-ATPase, likely by an indirect mechanism that involves an increase of intracellular sodium concentration; and (2) the relaxant phase of 5-HT-evoked vasoactive responses is not mediated by the release of nitric oxide or prostacyclin from the endothelium.
 ...
PMID:Sodium pump activation by 5-hydroxytryptamine in human placental veins. 133 Jun 19

Thapsigargin, which acts by inhibition of a Ca(++)-ATPase on the dense tubule system in platelets, is a pharmacological tool to study the effects of increases in intracellular Ca++. Secondary consequences of thapsigargin treatment in platelets include extensive thromboxane B2 formation (493 +/- 106 ng/10(8) platelets) and [3H]5-hydroxytryptamine secretion (80.7 +/- 8.0%). Inhibition of cyclooxygenase by ibuprofen prevents thromboxane B2 formation (0.1 +/- 0.04 ng/10(8) platelets) and dense tubule secretion (6.5 +/- 3.8%). Aggregation in response to thapsigargin is rapid and maximal, but the rate and extent of aggregation are lowered by ibuprofen or aspirin. Mobilization of intracellular Ca++ is also significantly attenuated when eicosanoid formation is prevented, indicating the dependence of thapsigargin actions on endogenous lipid mediator formation. These studies also support the idea that formation of endogenous thromboxane A2/prostaglandin H2 is self-amplifying; thromboxane receptor antagonists inhibit endogenous thromboxane B2 formation, indicating that Ca(++)-dependent activation of phospholipase A2 is only partially responsible for eicosanoid production. Our data indicate the importance of distinguishing secondary effects of thapsigargin, especially because it may influence eicosanoid formation.
 ...
PMID:Indirect actions of thapsigargin on human platelets: activation of eicosanoid biosynthesis and cellular signaling pathways. 153 33


1 2 3 4 5 6 7 8 Next >>