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)

1. Vascular contractions induced by K(+)-free solution and relaxation responses following the return of K+ to the organ bath were studied in mesenteric arterial rings from spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY) with particular focus on the role of vascular adrenergic nerve-endings and endothelium. 2. In endothelium-denuded rings the omission of K+ from the incubation medium resulted in gradual contractions, the rate of which was slower in SHR than WKY. Nifedipine (1 microM) inhibited the contractions more effectively in SHR than WKY. 3. Adrenergic denervation in vitro with 6-hydroxydopamine reduced the contractions induced by the K(+)-free medium in endothelium-denuded rings. The remaining contractions after denervation were markedly greater in SHR than WKY. 4. The presence of intact vascular endothelium attenuated the K(+)-free contractions in both strains, the attenuation being smaller in SHR than WKY. NG-nitro-L-arginine methyl ester (L-NAME, 0.1 mM) and methylene blue (10 microM), but not indomethacin (10 microM), abolished the attenuating effect of endothelium on the K(+)-free contractions. L-Arginine (1 mM) reversed the effect of L-NAME in WKY but not in SHR. 5. The re-addition of K+ after full K(+)-free contractions dose-dependently relaxed the rings. The rate of this K(+)-induced relaxation was significantly slower in SHR than WKY at all K+ concentrations (0.1-5.9 mM) studied, whether the endothelium or functioning adrenergic nerve-endings were present or not. Ouabain (1 mM) totally inhibited the K+ relaxation in SHR but only partially in WKY.6. Vascular smooth muscle contractions induced by high concentrations of potassium were comparable between the strains. The EC50 for noradrenaline-induced contractions was lower in SHR than WKY, but the maximal forces did not differ significantly.7. In conclusion, the contractile response in K+-free solution more clearly differentiates vascular rings from SHR and WKY than the responses induced by the classical contractile agents noradrenaline and high concentrations of potassium. The depressant effect of the presence of intact endothelium on the K+-free contractions, which was smaller in SHR than WKY, is mediated via the endothelium-derived relaxing factor. Neurotransmitter release from vascular adrenergic nerve-endings participates less in the K+-free contractile response in SHR than WKY. Moreover, the contractile response is more dependent on calcium entry through nifedipine-sensitive calcium channels in SHR than WKY. The greater K+-free contractions of denervated endothelium-denuded rings and the reduced K+ relaxation rate in SHR when compared to WKY suggest increased cell membrane permeability and decreased activity of vascular Na+, K+-ATPase, respectively, in this type of genetic hypertension.
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PMID:Contractions induced by potassium-free solution and potassium relaxation in vascular smooth muscle of hypertensive and normotensive rats. 150 24

The effect of a bufodienolide (monohydroxy-14,15-epoxy-20,22-dienolide glycoside) purified from toad skin was compared with that of ouabain on 3H-noradrenaline release and on the tension of rabbit pulmonary arterial strips. This compound exerted an ouabain-like activity. The neuronal effects of this bufodienolide derivative on squid axon were also studied and compared with those of ouabain. Both compounds enhanced the resting and stimulation-evoked (2 Hz, 360 shocks) release of 3H-noradrenaline. Moreover, in the presence of either this bufodienolide or ouabain, the tension of the rabbit artery increased gradually, and the contraction evoked by electrical stimulation was potentiated. Both compounds enhanced, in a prazosin-sensitive way, smooth muscle responses to noradrenaline and to electrical stimulation. In higher concentrations, they contracted smooth muscle cells of pulmonary artery, an action which was insensitive to prazosin. The bufodienolide was about 8 times more active in inhibition of 22Na efflux than was ouabain, but did not affect Ca efflux, which is not sensitive to ouabain. It is therefore concluded that compounds with an inhibitory effect on Na+,K(+)-ATPase are able to affect chemical neurotransmission of blood vessels in such a way that in lower concentrations they potentiate the release of noradrenaline, and in higher concentrations they contract directly the smooth muscle. These findings indicate that such compounds if they are present in the circulation might be involved in the physiological regulation of blood pressure or in the genesis of hypertension.
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PMID:Comparison of the effects of a bufodienolide and ouabain on neuronal and smooth muscle preparations. 165 19

1. The contractile responses of aortic ring preparations from Sprague-Dawley rats made hypertensive by 6-week dietary salt loading were studied. The test and control diet contained 8.0 and 0.3% NaCl, respectively. Aortic rings from salt-loaded rats showed enhanced sensitivity to noradrenaline (NA) but not to serotonin. Contractile responses to CaCl2 in Ca-free NA-containing medium was significantly enhanced in salt-loaded rats, but was unchanged in K(+)-depolarised medium. K(+)-induced relaxation (a functional indicator of Na-K adenosine triphosphatase activity) was sensitive to 10 mumol/L ouabain and was significantly attenuated in aortic rings from salt-loaded rats. The results suggest that hypertension induced by salt-loading is associated with enhanced sensitivity to NA, increased Ca2+ entry through receptor-operated channels, and impairment of Na-K ATPase enzyme activity.
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PMID:Altered responses of aortic smooth muscle from Sprague-Dawley rats with salt-induced hypertension. 166 59

1. Acetylcholine (ACh), 7.5 x 10(-5) M, and carbachol, 5 x 10(-6) M (CCh) depressed the frequency of miniature endplate potentials (m.e.p.ps) in the frog (Rana temporaria) sartorius neuromuscular junction with active acetylcholinesterase to about 50-55% of the controls. 2. A similar depression was produced by the nicotinic agonists, nicotine, suberyldicholine and tetramethylammonium. 3. The muscarinic agonists, oxotremorine, methylfurmethide and methacholine were without effect on m.e.p.p. frequency. The muscarinic antagonist, atropine and the nicotinic antagonist, (+)-tubocurarine, had no effect on the depression of m.e.p.p. frequency evoked by CCh. 4. The ganglionic blockers, benzhexonium and IEM-1119, were also without effect on the CCh-evoked depression of m.e.p.p. frequency. 5. Pretreatment of muscles with anticholinesterases did not prevent the CCh-induced drop in m.e.p.p. frequency. 6. The effect of CCh was proportionally the same as in the controls in preparations where the m.e.p.p. frequency was changed by elevation of K+ and in the presence of theophylline, noradrenaline, dibutyryl adenosine 3':5'-cyclic monophosphate (db cyclic AMP) and db cyclic GMP. 7. An inhibitor of Na+,K(+)-ATPase, ouabain, 5 x 10(-5) mol l-1, prevented or reversed the depression of m.e.p.p. frequency by CCh. However, the depression was present in a nominally K(+)-free medium. Insulin and adrenaline, which are considered to be Na+,K(+)-ATPase activators, were without effect on depression of m.e.p.p. frequency. 8. The depression of m.e.p.p. frequency by 5 x 10(-6) M CCh was the same at temperatures between 5 and 30 degrees C with a Q10 near to 1.0. When threshold amounts of CCh were used (6 x 10-7 and 3 x 10-7 M), the depression was less at higher temperatures.9. The receptive structures responsible for the CCh (or ACh)-evoked depression of m.e.p.p. frequency differ pharmacologically from muscarinic, nicotinic ganglionic and neuromuscular junction ACh-receptors as well as from the synaptic cholinesterase, in contrast to previous reports (Duncan & Publicover, 1979).The low temperature-dependence points to the possibility that physical rather than biochemical processes are limiting in this presynaptic effect of cholinomimetics.
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PMID:Depression of miniature endplate potential frequency by acetylcholine and its analogues in frog. 166 83

1. Sodium nitroprusside (NP) caused both an inhibition of a noradrenaline (NA)-induced contraction and an elevation of cyclic guanosine 3',5'-monophosphate (cyclic GMP) in rat aorta. Both NP-induced responses were enhanced by the selective cyclic GMP phosphodiesterase inhibitor, M&B 22948 (2-o-propoxyphenyl-8-aza-purin-6-one, 30 microM). 2. The inhibition of a NA-induced contraction by NP was characterized by dissociating the intracellular Ca2+ release component from the extracellular Ca2+ influx component of the contraction. The transient contraction stimulated by NA in the absence of extracellular Ca2+ was inhibited by NP. Also, the slowly developed tension stimulated by NA in aortas depleted of stored Ca2+ and subsequently exposed to extracellular Ca2+ was inhibited by NP. Both components of contraction were equally sensitive to NP. 3. NA stimulated both unidirectional 45Ca2+ influx in the presence of extracellular Ca2+ and 45Ca2+ efflux into a 0 Ca2+ solution that contained 2 mM-ethyleneglycol-bis-(beta-aminoethylether)N,N'-tetraacetic acid (EGTA). The increased 45Ca2+ efflux is thought to reflect release of stored Ca2+ followed by membrane transport. NP greater than 10 nM inhibited both 45Ca2+ influx and release components whereas NP at 1-3 nM enhanced NA-stimulated 45Ca2+ efflux and relaxed the maintained tension caused by NA in 0 Ca2+, 2 mM-EGTA. 4. NP also inhibited the Ca2(+)-dependent 42K+ and 36Cl- effluxes from rat aorta stimulated either by NA or by high potassium. NP inhibited the contractile and flux responses to NA more effectively than the responses to high potassium. 5. These data indicate that: (1) NP reduces cytosolic Ca2+ by the combined inhibitory effects on Ca2+ influx and intracellular Ca2+ release, and by the stimulation of a Ca2(+)-ATPase; and (2) the differential sensitivity of the NA and high-potassium responses to NP may reflect underlying differences in Ca2+ handling induced by receptor occupancy and depolarization.
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PMID:Sodium nitroprusside alters Ca2+ flux components and Ca2(+)-dependent fluxes of K+ and Cl- in rat aorta. 169

Physical activity and pharmacological stimulation of beta 2-adrenoceptors by salbutamol increase skeletal muscle digoxin binding with a secondary decrease in serum digoxin, possibly due to increased Na-K-ATPase activity. The present study was undertaken to examine if adrenaline (ADR) infusion and sympathoadrenal stimulation by mental stress affect the serum concentrations of digoxin and potassium. After 10 days on 0.50 mg digoxin orally, 35 healthy volunteers were investigated following 2 h of supine rest. They were divided into four groups: intravenous saline (placebo, n = 10). ADR infusion at the rates of 0.1 nmol kg-1 min-1 (ADR-L, n = 8), 0.4 nmol kg-1 min-1 (ADR-H, n = 7), or subjected to a mental stress [a color-word conflict test (CWT), n = 10]. Arterial blood samples were taken before and during the active period (50 min) and during the following 60 min (at rest) to analyze serum digoxin and potassium and plasma ADR and noradrenaline (NA). All variables were stable during placebo infusion. ADR infusions caused significant and dose-dependent decreases in serum digoxin (p less than 0.05 during ADR-L and p less than 0.001 during ADR-H) and serum potassium (p less than 0.05 and p less than 0.001, respectively). CWT, on the other hand, did not reduce serum digoxin and caused a slight decrease in serum potassium only in the poststress period. Thus, ADR caused dose-dependent shifts of digoxin and potassium, whereas mental stress failed to do so, possibly due to a modest ADR response and small increases in sympathetic nerve activity in skeletal muscle.
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PMID:Effects of adrenaline and mental stress on serum digoxin concentration. 170 39

1. When the web of the anaesthetized Xenopus laevis was perfused with Ringer solution maintained at 20 degrees C, radio frequency (RF) burst-type electromagnetic (EM) field radiation not only dilated arterioles of the web which had been preconstricted with noradrenaline, but also dilated arterioles under non-stimulated conditions. The EM field-induced vasodilatation increased slowly and reached a plateau 60 min after the onset of radiation. After the cessation of radiation, vasodilatation remained for 10-20 min, then slowly subsided. 2. When a 10 MHz, 1 V (peak to peak) generator voltage induced a 7.3 milliGauss, 2.19 V cm-1 EM field, the vasodilatory effect was optimum when bursts were applied 50% of the total time at 10 kHz burst rate. 3. The vasodilatory effect was not secondary to dielectric heat in the web, because the EM field was too weak to have produced enough heat to dilate the arterioles and heat would have been constantly conducted away by the perfusion solution. 4. During perfusion with Ringer solution warmed to 30 degrees C, no vasodilatation was found, but perfusion with Ringer solution warmed to 35 degrees C induced only 11% vasodilatation. Perfusion with Ringer solution warmed to 37 degrees C induced irreversible vasoconstriction. The pattern of vasodilatation induced by warm Ringer solution was different from the vasodilatory effect of weak EM field radiation. 5. The extent of the vasodilatory effect was influenced by Ca2+ concentration of the perfusion medium. Under normal Ca2+ conditions arterioles dilated to 126% of the control diameter, while under Ca(2+)-free conditions arterioles dilated to 131% of the control value and under high-Ca2+ conditions (twice the normal level) arterioles dilated to 111% of the control value. This suggests that the vasodilatory effect may be caused by facilitation of Ca2+ outflow, and the extent of this flow may settle down to the equilibrium level of countercurrent flux between Ca2+ influx and outflow. 6. The vasodilatory effect was not inhibited under perfusion with Na(+)-free Ringer solution, suggesting that Na(+)-Ca2+ exchange system may not be involved in the vasodilatory effect. The vasodilatory effect was inhibited by vanadate, an inhibitor of Ca(2+)-ATPase, and was abolished by Methylene Blue, an inhibitor of guanylate cyclase. The evidence suggests that the mechanism of the vasodilatory effect may depend on an increase in Ca2+ outflow through the plasma membrane of the smooth muscle and/or an increase in Ca2+ influx into the sarcoplasmic reticulum.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Non-thermal vasodilatation by radio frequency burst-type electromagnetic field radiation in the frog. 177 Apr 39

Essential hypertension is primarily hereditary. The property inherited is present in all cells but because of adaptation and differentiation it is particularly prominent in systemic vascular smooth muscle. This inherited property is manifested functionally as increased reactivity to vasoactive substances, such as (-)noradrenaline and angiotensin II. This abnormal function is present before the onset of hypertension. Vascular hypertrophy and hyperplasia are not only caused by hyperactivity of the smooth muscle and by the hypertension itself but are also trophic effect of the agonists, especially noradrenaline. The only two proteins in vascular smooth muscle which can produce both contractile and trophic effects are the guanosine triphosphate binding protein (Gs) and phospholipase C. Phospholipase C has already been demonstrated to be abnormally active in response to agonists in the spontaneously hypertensive rat and in human essential hypertension. The Gs protein is less likely to be critically abnormal since it is active in the vascular smooth muscle relaxation cascade as well as in contraction. None of the other proteins involved in vascular smooth muscle contraction or relaxation affect both contractile reactivity and cellular growth. There are many secondary effects dependent upon the phospholipase C abnormality such as calcium (Ca2+) cellular content, Ca2+ Mg2+ ATPase pump effects and possibly Ca2+ Na+ exchange. There are also many secondary effects impinging on the phospholipase C abnormality including changes in noradrenaline and angiotensin II metabolism. Present antihypertensive therapy is directed largely at secondary factors dependent upon or influencing the primary phospholipase C cascade. The path is now open for a more direct and basic diagnostic and therapeutic attack.
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PMID:The aetiology of essential hypertension. 177 Apr 74

The effects of morphine on noradrenaline (NA) release from rat cerebrocortical synaptosomes and on the synaptosomal Na+,K(+)-ATPase activity were determined. Morphine (10(-3)-10(-5) M) caused a dose-related inhibition of enhanced prelabelled [3H]NA release evoked by a high concentration of K+ from synaptosomes and this inhibitory action of morphine was antagonized by the specific antagonist naloxone (10(-4), 10(-5) M). Morphine dose-dependently stimulated the synaptosomal Na+,K(+)-ATPase activity but not Ca2(+)-ATPase activity in the incubation medium containing 2.2 x 10(-6)-4.7 x 10(-7) M free Ca2+, and this stimulatory effect was antagonized by naloxone. These results suggest that morphine may have some role in the suppression of membrane depolarization and/or the release of NA through its stimulatory action on the Na+,K(+)-ATPase activity in rat cerebral cortex.
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PMID:Inhibition of noradrenaline release from cerebrocortical synaptosomes and stimulation of synaptosomal Na+,K(+)-ATPase activity by morphine in rats. 196 57

Factors regulating the activity of synaptosomal Na, K-ATPase have been found in the cytosol of nerve endings. The activatory effect of the factor increases in the presence of neurotransmitters regardless of their direct action on Na, K-ATPase. Synaptosomal Na, K-ATPase is not sensitive to the factor obtained from the cytosol of kidney tissue, or the cytosolic fraction obtained after sedimentation of microsomes. The effect of inhibiting low molecular ET(S) fraction on Na, K-ATPase activity is not mediated through noradrenaline, dopamine and serotonin as well by the system of secondary messengers. Factor stimulated by neurotransmitters activates the Na, K-ATPase system affecting the phosphorylating intermediates of the enzyme and putting the Na, K-ATPase system in the mode of simultaneous transport of Na and K ions.
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PMID:[The regulation of the Na, K-ATPase system by neurotransmitters]. 197 88


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