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)

Isoproterenol or forskolin induce a 10-15-fold increase in concentration of cyclic AMP in rat reticulocytes as compared with the basal level of 2.3 +/- 0.3 microM. Glycolysis is stimulated by both compounds transiently more than 2-fold with a peak after 7.5 min followed by an exponential decline. The glycolytic rate in the presence of 10 microM isoproterenol or 10 microM forskolin did not return to basal levels within 60 min of incubation, but was depressed by as much as 50% under the influence of 100 microM forskolin. This phenomenon is designated as metabolic desensitization. The stimulation of glycolysis is probably due to activation of phosphofructokinase as well as to stimulation of Na+,K+-ATPase. The diminished glycolytic flux during the period of metabolic desensitization is accompanied by a decline of glucose 6-phosphate and in the presence of high concentrations of forskolin also by a decrease in glucose 1,6-bisphosphate. A lower rate of influx of glucose is postulated.
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PMID:Activation and desensitization of glycolysis by stimulation of adenylate cyclase in rat reticulocytes. 243 74

Some aspects of the genetic and non-genetic control of the amount and rate of calcium cycled during steady-state activation of papillary muscles from right ventricular rabbit myocardium are presented. Genetic reorganization of the intracellular structure of the myocardium is achieved by producing right ventricular pressure overload and thyrotoxic hypertrophy. The mechanical performance of the pressure overload heart is slowed while time to peak tension is increased. These changes are associated with an increase in myothermal economy. In thyrotoxic hypertrophy the rate of mechanical performance is increased while time to peak tension is decreased. These alterations are associated with a decrease in myothermal economy. Tension-independent heat is used as an index of calcium cycling. In pressure overload hearts the amount and rate of calcium cycling is decreased. In contrast in thyrotoxic hypertrophy the amount of calcium cycled is unchanged while the rate is increased. In the pressure overload hearts there is a decrease in sarcoplasmic reticular (SR) Ca++ ATPase, whereas in the thyrotoxic preparations the message is increased. The change in the rate of calcium uptake in pressure overload and thyrotoxic hearts is correlated with a change in the amount of SR Ca++ ATPase mRNA. Calcium cycling was also altered by non-genetic inotropic intervention. Isoproterenol (1 microM) increases the amount of calcium cycled during each contraction relaxation cycle and the rate at which it is removed. These alterations are associated with an increase in force and a foreshortened twitch. Incubating the papillary muscle in high calcium (11 mM) also increases the force and the amount of calcium released into the cytosol. Under these circumstances the rate of uptake is not significantly increased and, accordingly, the isometric twitch is not foreshortened. In the presence of verapamil (14 microM) the peak twitch force is decreased and the isometric myogram is foreshortened. These changes are associated with a decrease in the amount of calcium released during activation and the rate at which it is removed.
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PMID:Genetic and non-genetic control of myocardial calcium. 253 Sep 77

To explore biochemical and functional differences between principal (PC) and intercalated cells (ICC), we have developed a method for separating them from rabbit kidney. Fragments of cortical collecting ducts were isolated by immunodissection, and single cells obtained from these clusters were stained with fluorochrome-conjugated, cell-specific markers. PC and ICC were then separated by fluorescence-activated cell sorting. Identity of the sorted cells was confirmed by staining with other cell-specific monoclonal antibodies (MCABs) or peanut lectin. Purity was greater than 99% for ICC and greater than 96% for PC. Arginine vasopressin (AVP) increased adenosine 3',5'-cyclic monophosphate (cAMP) accumulation in both cell types, but maximal stimulation was significantly greater with PC (approximately 20-fold) than with ICC (2.7-fold). Half-maximal stimulation was seen at approximately 2 x 10(-10) M AVP with both cell types. Isoproterenol increased cAMP levels only with ICC (from 1.23 +/- 0.16 to 12.06 +/- 1.25 fmol/cell; P less than 0.001). The number of ouabain binding sites and the activity of Na+-K+-ATPase was significantly higher in sorted PC than ICC (2.2 X 10(6) vs. 9.6 X 10(5) binding sites; 19.2 vs. 9.6 fmol.min-1.cell-1 ATP hydrolyzed in PC vs. ICC, respectively). These results demonstrate the feasibility of isolating homogeneous populations of PC and ICC, which is useful for further studies of their biochemical and functional characterization.
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PMID:Isolated principal and intercalated cells: hormone responsiveness and Na+-K+-ATPase activity. 253 51

Stimulation by serum of cell proliferation in G1-arrested culture of Chinese hamster ovary cells CHO-K1 was accompanied by an early (during the first minutes) and delayed (2-10 h) activation of Na+,K+-ATPase and an increase in cell K+ content from 0.5-0.6 to 0.7-0.8 mmol per gram protein. Isoproterenol acted synergistically with serum in eliciting both early and delayed changes in K+ transport and in stimulating G1----S transition. Isoproterenol alone (without serum) induced a transient increase in K+ influx via Na+,K+-ATPase without changing the cell K+ content or having any mitogenic effect. Theophylline enhanced the serum-induced early activation of Na+,K+-ATPase but inhibited both the delayed increase in cell K+ and the G1----S transition. Early serum-induced increase in K+ transport was not affected by cycloheximide, whereas net accumulation of cell K+ was abolished by the drug. It is concluded that the early and the delayed activation of Na+,K+-ATPase induced by mitogens can be dissociated; the early ionic response is related to the primary transduction of membrane signal, whereas the delayed modulation of ion transport via Na+,K+-ATPase has another function and is associated with cell growth.
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PMID:Early and delayed changes in potassium transport during the initiation of cell proliferation in CHO culture. 254 16

Active ion transport by the airway epithelium plays an important role in maintaining the effective defense mechanisms of the airway by regulating the volume and composition of the airway fluid. We investigated the abilities of adrenergic agents, cholinergic agents, and chemical mediators to modulate ion transport in canine tracheal epithelium, using Ussing-type chambers. Transepithelial electric potential difference (PD), resistance (R), and short circuit current (SCC) of the tracheal epithelium were measured before and during exposure to a drug or after a change in the perfusate composition. The mean values and S.E. (N = 41) of PD, R, and SCC during the control period were -18 +/- 4 mV (luminal negative to submucosa), 240 +/- 42 omega.cm2, and 50 +/- 5 microA/cm2, respectively. Ouabain (10(-4) M), an inhibitor of Na+-K+-ATPase, in the mucosal bath abolished PD and SCC. Replacement of luminal Na by choline reversibly reduced PD and SCC. These findings suggest that PD and SCC of the tracheal epithelium are maintained by the transcellular transport of luminal Na toward the mucosa. Isoproterenol (10(-5) M), epinephrine (10(-4) M), and norepinephrine (10(-4) M) markedly increased both PD and SCC. Acetylcholine (10(-4) M) and histamine (10(-4) M) did not alter SCC significantly. Prostaglandin E1 (10(-6) M) and F2 alpha (10(-5) M) slightly increased PD and SCC. These results indicate that adrenergic and cholinergic agents induce different patterns of effect on ion transport (adrenergic-dominant) in the tracheal epithelium. Thus, the effects of autonomic agents and chemical mediators on ion transport may explain, in part, the pathogenesis of airway disorders observed in many respiratory diseases.
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PMID:Effects of autonomic agents and chemical mediators on ion transport by canine tracheal epithelium. 279 19

The biological properties of Thromboxane B2 (TXB2) on isolated rat heart were studied. Its actions were compared with U-46619 a Thromboxane A2 mimetic compound and with isoproterenol. TXB2 induced a concentration-dependent increase in contractility, that was non-competitively antagonized by propranolol. In addition TXB2 inhibited Na+ + K+-ATPase activity at the same concentrations that influenced the mechanical activity. Inhibition of beta-adrenoceptors efficiently blocked the inhibitory action of TXB2 upon Na+ + K+-ATPase-activity. Isoproterenol simulated the positive inotropic effect and the inhibitory action of TXB2 on Na+ + K+-ATPase-activity. In contrast, U-46619 did not alter the basal dF/dt, neither the enzyme activity. The foregoing results suggest that TXB2 resembles the biological effect of catecholamines-inducing stimulation of myocardial contractility and inhibition of Na+ + K+-ATPase activity.
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PMID:TXB2: cardiostimulant effect that involves beta-adrenoceptor and Na+ + K+-ATPase activity. 284

The effect of anti beta adrenoceptor IgG from chagasic sera upon Ca2+-ATPase and Na++K+-ATPase of myocardial membrane was studied. Chagasic IgG stimulated Ca2+-ATPase and inhibited Na++K+-ATPase activities. Both enzymatic effects of the IgG could be prevented after beta adrenoceptor blockade or after the absorption of chagasic IgG with turkey red blood cells. Isoproterenol acted similarly. These results provide information concerning to the biochemical mechanism, by which an antibody, known to activate adenylate cyclase system coupled to cardiac beta adrenoceptor, produces stimulation of myocardial contractility.
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PMID:Chagasic IgG modifies the activity of sarcolemmal ATPases through a beta adrenergic mechanism. 288 Feb 70

The effects of tricyclohexyltin hydroxide (Plictran), an organotin acaricide, on 45Ca2+ uptake and Ca2+ ATPase were studied in vitro and in vivo in rat heart ventricular membrane vesicles, primarily sarcoplasmic reticulum. There was a concentration dependent inhibition of both 45Ca2+ uptake and Ca2+ ATPase in vivo as well as in vitro. Isoproterenol, a beta-adrenergic agonist, stimulated 45Ca2+ uptake and Ca2+ ATPase of sarcoplasmic reticulum and this was also inhibited by Plictran. Since cardiac relaxation is mediated by beta-adrenergic stimulation via Ca+ uptake by sarcoplasmic reticulum, the inhibition of calcium pump activity by Plictran may result in alterations in cardiac Ca2+ fluxes leading to cardiac dysfunction.
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PMID:Inhibition of beta-adrenergic stimulated calcium pump of rat cardiac sarcoplasmic reticulum by tricyclohexyltin hydroxide. 295 2

Calcium-independent regulation of the contractile proteins of cardiac muscle has been studied using hyperpermeable cells from rat ventricles and sections of quickly frozen rat hearts. These preparations have been used to study maximum Ca-activated force, myosin ATPase activity and the maximum velocity of unloaded shortening. Beta adrenergic activity increases the amount of force and the ATPase activity in accordance with the concentration of the V1 isozyme of myosin. V3 activity is decreased at the same time. In tissues containing only V1, there is no change in maximum velocity in response to beta adrenergic stimulation. These results indicate that beta adrenergic stimulation recruits V1 force generators and probably regulates a transition between a Ca unresponsive and a Ca responsive force generator. A 21,000 dalton protein that reproduces the effect of beta adrenergic stimulation on myosin has been isolated.
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PMID:Ca-independent regulation of cardiac myosin. 297 Feb 4

The mechanism of isoproterenol-induced inhibition of potassium release from rat parotid slices has been determined. Spontaneous potassium release from the slices was significantly inhibited by isoproterenol at concentrations above 10(-6) M. This isoproterenol effect was completely abolished in the presence of propranolol (10(-5) M) and ouabain (10(-3) M) and was abolished during Na+-exclusion from the incubation medium. Isoproterenol caused an enhancement of the microsomal Na+, K+-ATPase activity at concentrations above 10(-5) M, and this activity was inhibited by propranolol (10(-5) M). The stimulatory effect of isoproterenol on the Na+, K+-ATPase exhibited a strong correlation with the inhibition of potassium release on each dose of isoproterenol. Moreover, dibutyryl cyclic AMP at concentrations above 10(-4) M inhibited potassium release in a dose-dependent manner and cyclic AMP caused an enhancement of the microsomal Na+, K+-ATPase activity. These results suggest that the inhibitory effect of isoproterenol on potassium release is clearly derived from the elevated Na+, K+-ATPase activity and that it may in part be mediated by cyclic AMP.
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PMID:Isoproterenol inhibition of potassium release from rat parotid gland. 299 27


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