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

---

Query: EC:3.6.1.3 (ATPase)
65,361 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Effect in vitro of benthiocarb, an organocarbamate herbicide on neonate rat (3 day old) brain was studied to understand the interaction of benthiocarb with Na+K+-ATPase. Na+K+-ATPase of the developing rat brain was selected as an index enzyme since alterations in the Na+K+-ATPase activity leads to neuronal dysfunction. The assay of Na+K+-ATPase in the presence of 1-8 mu moles of benthiocarb showed decreased activity and a concentration dependent inhibition of Na+K+-ATPase was noticed upto 7 mu moles of benthiocarb. Based on IC50 values (median concentration), 50% inhibition of the enzyme was observed with 5 mu moles of benthiocarb. Norepinephrine (NE) was selected to study the modulation of benthiocarb inhibited enzyme. Maximum increase (76.7%) of Na+K+-ATPase was noticed with 35 mu moles of NE and effective concentration (EC50) of NE which produced 50% activation of the enzyme was found to be 20 mu moles. This study suggests that NE acts as a protective agent in reversing the benthiocarb in vitro inhibited neonate rat brain Na+K+-ATPase.
...
PMID:Modulation of benthiocarb in vitro inhibited neonate rat (Wistar strain) brain Na+K+-ATPase by norepinephrine. 255 4

Genetic hypertension in the rat is associated with abnormal renal function. This may be due to systemic hypertension or to intrinsic alterations in the kidney. Therefore, we examined intrinsic rates of oxidative metabolism in renal cortical tubules isolated from spontaneously hypertensive rats (SHR) and age-matched normotensive controls (WKY) before, during, and after the development of hypertension. We examined tubule function in SHR and WKY treated with antihypertensive agents to block the development of hypertension. During the early phase of hypertension (ages 7-8 wk), SHR tubules have intrinsic rates of oxygen consumption that are 15-25% greater than that of WKY. Ouabain-sensitive rates of oxygen consumption, an index of sodium entry, and Na+-K+-ATPase activity were not increased by 17%. Reduction of blood pressure with drugs did not abolish these differences in oxidative metabolism. Addition of exogenous arachidonic acid (1 microM) did reduce the metabolic differences between 8-wk-old SHR and WKY tubules. Norepinephrine (1 microM) had a greater stimulatory effect on oxygen consumption rates in tubules from hypertensive SHR. The relationship of these metabolic differences to the development of hypertension remains unclear.
...
PMID:Increased oxidative metabolism in renal tubules from spontaneously hypertensive rats. 258 84

The purpose of the present study is to determine the role of Na+,K+-ATPase in adrenergic neurotransmission of hypertension. Isolated perfused mesenteric vasculatures were prepared from spontaneously hypertensive rats (SHR, Okamoto and Aoki, 7-10 weeks old) and age-matched normotensive Wistar Kyoto rats (WKY). The effects of ouabain, a Na+,K+-ATPase inhibitor, on the norepinephrine overflow from the sympathetic nerve endings were examined. Norepinephrine overflow from the nerve endings as well as pressor responses during electrical nerve stimulation were significantly greater in SHR than in WKY. Ouabain increased the norepinephrine overflow evoked by electrical nerve stimulation, even in the presence of an uptake-blocker of norepinephrine. Further, the facilitatory effect of ouabain on stimulation-induced norepinephrine overflow was more prominent in SHR than in WKY. These results suggested that ouabain-sensitive Na+,K+-ATPase on sympathetic nerve terminals could have an important role in the regulation of neurotransmitter release, and that its activity might be enhanced in SHR compared with WKY.
...
PMID:Effects of ouabain on adrenergic neurotransmission in spontaneously hypertensive rats. 283 72

Noradrenaline potently antagonizes the effects of N-methyl-D-aspartate (NMDA) (80 microM) on cyclic GMP production in immature rat cerebellar slices in vitro (IC50 = 0.6 microM). The effect is stereospecific (D-noradrenaline, IC50 = 100 microM), and also observed with adrenaline (IC50 = 0.5 microM) and isoprenaline (IC50 = 1.2 microM). The alpha 1-adrenoceptor agonists methoxamine or phenylephrine or the mixed alpha 1/alpha 2 agonists oxymetazoline or xylometazoline (100 microM) do not block the effects of NMDA, but the alpha 2-adrenoceptor agonist clonidine is weakly active (IC50 = 200 microM). Salbutamol and terbutaline were also inactive except at high concentrations (300 microM), as were a number of other catechol and phenylethylamine derivatives. The antagonistic effects of noradrenaline on the NMDA response were insensitive to phentolamine, atenolol, or propranolol (up to 100 microM), but were blocked by the alpha 2 antagonist idazoxan (1-10 microM). The Na+,K+-ATPase inhibitor ouabain (0.1-10 microM) markedly potentiates the effects of NMDA in this model, and also antagonizes and reverses the ability of noradrenaline (10 microM) to block the effects of NMDA. The results suggest that noradrenaline and Na+,K+-ATPase activity have potent modulatory effects on the NMDA response.
...
PMID:Noradrenaline antagonizes and ouabain potentiates the effects of N-methyl-D-aspartate on rat cerebellar cyclic GMP production. 284 58

Norepinephrine (NE) sensitization of rat brain Na+ -K+ ATPase to ethanol (EtOH) inhibition appears to be mediated by alpha 1-adrenoreceptors, since it was reversed by prazosin and WB-4101 (alpha 1-receptor antagonists) in a concentration-dependent manner, but not by yohimbine and piperoxan (alpha 2-receptor antagonists). In addition, clonidine (alpha 2-agonist) and methoxamine (central receptor type uncertain) produced very little sensitization. Chronic EtOH administration to rats for 3 weeks produced tolerance to the hypothermic effect of test doses of EtOH (3 g/kg, i.p.) and a decreased inhibitory effect of NE + EtOH on the enzyme in vitro. This inhibition was still prevented by prazosin and WB-4101. However, the binding of tritiated WB-4101 and prazosin to brain membrane preparations from control and EtOH-tolerant rats revealed that the maximum number of binding sites (Bmax) and the dissociation constant (KD) of alpha 1-adrenoreceptors were decreased after tolerance development. These changes in numbers and binding properties of alpha 1-adrenoreceptors probably account for the decreased NE sensitization of the ATPase to EtOH inhibition in preparations from EtOH-tolerant rats.
...
PMID:Alpha 1-adrenergic receptor involvement in norepinephrine-ethanol inhibition of rat brain Na+ -K+ ATPase and in ethanol tolerance. 286 93

Vanadate (+5) is a potent inhibitor of a variety of ATPases including dynein ATPase. We describe a method useful for estimating the functional dissociation rate of vanadate from the active site which does not rely on classical physical separation techniques. The method involves spectrophotometrically monitoring the enzymatic activity as the inhibitor dissociates from the enzyme and is inactivated by norepinephrine. Norepinephrine effectively reverses vanadate inhibition by reducing vanadate (+5) to oxovanadium (+4). This reduction by norepinephrine is sufficiently fast for these purposes--addition of vanadate after norepinephrine shows no inhibition of ATPase activity. The mathematical estimation procedure is generally useful for estimation of dissociation rates of other reversible inhibitors which can be quickly inactivated after dissociation from the enzyme. The rate of dissociation of vanadate from dynein with ATP and 2-N3ATP as substrates using this method was estimated to be in the ranges 0.0023-0.0042 and 0.0057-0.0075 s-1, respectively. These rates permit estimation of the rates of vanadate association with dynein by using the reported dissociation constant for vanadate. The results are consistent with the very fast and potent inhibition of dynein ATPase activity observed.
...
PMID:Kinetics of vanadate dissociation: estimation of the rate by inhibitor inactivation. 296 96

Norepinephrine (0.1 mM) has been reported to "sensitize" (Na+ + K+)-ATPase activity of rat brain homogenates to inhibition by ethanol. The present study extends these investigations to the mouse and includes other ATPase activities. We measured the effects of norepinephrine on the sensitivity of ethanol-induced inhibition of (Na+ + K+)-stimulated (E.C. 3.6.1.3), (Mg++)-dependent (E.C. 3.6.1.4) and (Ca++)-dependent ATPase activities. Whole forebrains from C57BL/6J mice were homogenized and assayed in vitro for ATPase activity using standard conditions. Ethanol (0.125-2.0 M) caused a dose-dependent inhibition of all three ATPases. Norepinephrine (0.1 mM) had no appreciable effect on ethanol's inhibition of (Na+ + K+)-stimulated or (Ca++)-dependent ATPase activities, but slightly antagonized ethanol's effect on (Mg++)-ATPase. These results suggest that norepinephrine has little effect on the sensitivities of specific ATPases to ethanol inhibition in mouse brain.
...
PMID:Effect of norepinephrine on inhibition of mouse brain (Na+ + K+)-stimulated, (Mg++)-dependent, and (Ca++)-dependent ATPase activities by ethanol. 299 May

Inhibition of the Na,K-ATPase is known to cause transmitter release from many neurons. The mechanism of [3H]norepinephrine release was examined in primary cultures of sympathetic neurons. Ouabain caused [3H]norepinephrine release at concentrations that produced 80 to 90% inhibition of Na,K-ATPase activity. The effect of ouabain was compared with the effects of high K+ and the Ca2+ ionophore A23187. [3H]Norepinephrine release elicited by depolarization with high extracellular K+ was dependent on extracellular Ca2+, was unaffected by tetrodotoxin, was potentiated by reducing extracellular Na+, and was potentiated by the norepinephrine uptake inhibitor desipramine. These are the results expected if high K+ causes release by exocytosis, and if blockade of the Na+-dependent norepinephrine uptake system increases the net measurable release of the transmitter. The Ca2+ ionophore A23187 caused [3H]norepinephrine release that was not dependent on extracellular Ca2+ but which was like the release elicited by high K+ in other respects. Release elicited by ouabain was independent of extracellular Ca2+, was delayed for several hours by tetrodotoxin, was inhibited by reducing the concentration of extracellular Na+, and was inhibited by desipramine. These results suggest that the measured increase in transmitter release is secondary to a rise in the concentration of intracellular Na+. The data are consistent with the hypothesis that at high levels of pump inhibition, ouabain elicits nonvesicular [3H]norepinephrine release through reversal of the Na+-dependent plasma membrane carrier.
...
PMID:Ouabain-evoked norepinephrine release from intact rat sympathetic neurons: evidence for carrier-mediated release. 299 43

The mechanism by which noradrenaline stimulates ouabain-sensitive rubidium uptake in guinea-pig myocardial tissue has been studied. The stimulatory action of low concentrations of noradrenaline was reversed by high doses of propranolol (10(-5) mol/l) in atrial tissue, but was not reversed by alpha- or beta-, or combined alpha- and beta- adrenoceptor antagonists in ventricular tissue. Rubidium uptake was also found to increase with increasing extracellular potassium concentration [( K]o). The percentage values of stimulation by noradrenaline decreased with increasing [K]o. Noradrenaline had no effect on the rate of ATP splitting by an isolated membrane preparation of Na,K-ATPase. It is proposed that noradrenaline stimulates active cation transport by either (a) an effect secondary to increased passive efflux of K ions, or (b) an action at a novel adrenergic receptor, distinct from the ATPase enzyme itself.
...
PMID:The mechanisms of action of noradrenaline on ouabain-sensitive rubidium uptake in guinea-pig myocardium. 299 91

We examined effects of treatment with cardiac glycosides, in combination with noradrenergic stimulation or depletion, on (Na+,K+)-ATPase activity in rat cerebral cortex, heart, and kidney. Treatment with digitoxin increased the apparent number of (Na+,K+)-ATPase sites in heart, cerebral cortex, and kidney. Ouabain, which crosses the blood-brain barrier poorly, did not affect enzyme in brain but was otherwise similar. Norepinephrine depletion prevented the increase in heart but not in cerebral cortex. Noradrenergic stimulation increased the number of sites in cerebral cortex and in heart. In rats treated with digitoxin, noradrenergic stimulation increased enzyme activity further in heart but not in cerebral cortex. Examination of effects on noradrenergic receptor binding and on norepinephrine metabolite concentrations suggested that, while in heart cardiac glycosides appeared to increase norepinephrine release, in brain there was no effect on release but there may have been appreciable inhibition of norepinephrine reuptake under stimulated conditions.
...
PMID:(Na+,K+)-ATPase and noradrenergic regulation: effects of cardiac glycoside treatment and noradrenergic manipulations. 300 19


<< Previous 1 2 3 4 5 6 Next >>

---