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)

1 Intracellular potentials were recorded in driven left atria from reserpine-treated rabbits. Guanethidine 2 X 10(-5) M slightly increased Vmax and shortened the total duration (TD) of the action potential (AP) without causing hyperpolarization. For the first 30 min after 4 X 10(-4) M, Vmax increased without hyperpolarization and AP height increased slightly. Thereafter, Vmax and height decreased with a slight and gradual depolarization. This depolarization was irreversible. TD was increased after 15 minutes. Guanethidine 2 X 10(-3) M initially decreased Vmax and height before causing depolarization. 2. Pretreatment with tetrodotoxin (TTX) 1.6 X 10(-7) M prevented or reversed the initial increases in Vmax, height and TD induced by guanethidine (4 X 10(-4) M). 3 TTX 3.1 to 6.2 X 10(-6) M, added 15 or 30 min after guanethidine 4 X 10(-4) M, delayed or prevented depolarization by guanethidine. 4 Ouabain 10(-5) M incubated for 20 and 90 min greatly inhibited Na+, K+-adenosine triphosphatase and K+-phosphatase activities; guanethidine was without effect. 5 Guanethidine probably increases resting sodium permeability after the promotion of increases in sodium permeability during the AP. High doses of the drug decrease sodium permeability during the AP.
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PMID:Action of guanethidine on rabbit atrial membranes. 20 4

1. The endogenous noradrenaline content of cat spleen slices was markedly reduced when the slices were incubated at 37 degrees C in a medium in which sodium was replaced by sucrose, lithium, choline or potassium. Depletion of tissue noradrenaline was accounted for by its release into the incubating medium. At an external sodium concentration of 20 mM, about 50% depletion was obtained in 2 hours.2. The enhanced release induced by sodium deprivation occurred in the absence of calcium, with or without ethyleneglycol-bis (beta-aminoethyl ether) N,N' tetraacetic acid. Manganese potentiated release, while magnesium was without effect.3. Ouabain caused a dose-dependent release of noradrenaline which was partially calcium-dependent. Removal of potassium from the incubation medium caused some release, which was potentiated in 25 mM sodium Krebs solution or by ouabain.4. At 4 degrees C, the release did not occur in sodium-free medium.5. Dinitrophenol did not affect the loss of noradrenaline caused by sodium withdrawal. Iodoacetic acid and N-ethylmaleimide caused a time-dependent depletion of noradrenaline. Tetracaine caused release and partly opposed the release caused by sodium deprivation. Tetrodotoxin had no effect. Guanethidine, but not phenoxybenzamine, released noradrenaline and potentiated the release induced by sodium withdrawal.6. The rate of release of (3)H-noradrenaline from reserpine-treated spleen slices was not altered by sodium withdrawal.7. Uptake-retention of (3)H-noradrenaline in slices depleted of their endogenous noradrenaline content by sodium deprivation was about 60% of the control slices. This was effectively blocked by cocaine. Release of (3)H-noradrenaline evoked by high potassium from both control and treated slices was calcium-dependent.8. It is suggested that sodium-potassium-activated ATPase maintains the integrity of the axonal membrane, and any procedure which depresses the activity of the enzyme or the sodium-potassium pump would cause transmitter release by causing temporary disturbance in the membrane. Evidence is presented to suggest that vesicles depleted of their endogenous noradrenaline content by sodium deprivation are re-used for the storage and release of transmitter.
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PMID:Release of noradrenaline from the cat spleen by sodium deprivation. 412 79

Recently, we have shown that by releasing specific nucleotidases the sympathetic nerves of the guinea pig vas deferens may regulate the metabolism of extracellular adenine nucleotides and consequently, the inactivation of neurotransmitter ATP. Based on the evidence for tetrodotoxin sensitivity and calcium dependence of the nerve stimulation-evoked overflow of enzyme activity, we have suggested that soluble nucleotidases may be stored in synaptic vesicles within the sympathetic nerves and released upon arrival of nerve action potentials by a mechanism similar to that for release of neurotransmitters. To further test this hypothesis we studied the time course of nerve stimulation-evoked overflow of ATP, norepinephrine (NE), releasable ATPase (r-ATPase) activity, and releasable AMPase (r-AMPase) activity under control conditions and in the presence of drugs known to selectively modulate sympathetic neurotransmission. The results show that the time course of overflow of r-ATPase and r-AMPase activities resembles the transient pattern of overflow of ATP but not the tonic pattern of overflow of NE. Vasa deferentia dissected from animals treated with reserpine release ATP, r-ATPase, and r-AMPase, whereas the overflow of NE is completely abolished. Guanethidine, on the other hand, inhibits equally well the overflow of the two neurotransmitters and the releasable nucleotidase activities. Agonists of the alpha(2)-adrenergic receptors abolish the overflow of ATP, r- ATPase, and r-AMPase but not the overflow of NE. This evidence supports the idea that the sympathetic nerves of the guinea pig vas deferens store and release ATP together with specific nucleotidases responsible for the inactivation of this neurotransmitter.
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PMID:Correlation between the release of the sympathetic neurotransmitter ATP and soluble nucleotidases from the guinea pig vas deferens. 1112 63