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)

Isolated mouse vas deferens preparations were used to study the effect of temperature on noradrenaline-induced contractions. Preparations were suspended in the organ bath containing Krebs-Henseleit solution for isometric tension recording. Contractile responses to noradrenaline were investigated in the mouse vas deferens after moderate cooling from 37 to 26 or 22 degrees C. A significant increase of the phasic contractions to noradrenaline was observed at 26 or 22 degrees C compared with responses obtained at 37 degrees C (about 12.3 and 35.6% increase at 26 and 22 degrees C, respectively). The secondary noradrenaline-induced sustained contraction was also significantly enhanced after moderate cooling to 26 degrees C. The potentiation of noradrenaline-induced contraction at 26 degrees C remained in a Ca(2+)-free EGTA (1 mM)-containing solution. However, sustained contraction was suppressed after removal of the calcium from the medium at 37 and 26 degrees C. Contraction to caffeine was significantly enhanced at 22 degrees C compared with 37 degrees C. By contrast, barium chloride-induced contraction of the vas deferens was markedly decreased after moderate cooling to 22 degrees C. In the presence of ouabain (0.1 mM), the noradrenaline-induced peak contraction was significantly increased at 37 degrees C. However, potentiation of the noradrenaline response at 22 degrees C was unaffected by the Na+/K+ pump inhibitor. Noradrenaline-induced peak contractions were depressed in the presence of vanadate (1 mM) and cyclopiazonic acid (10 microM), two Ca(2+)-ATPase inhibitors, at 37 degrees C and also at 22 degrees C.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Effect of moderate cooling on contractile responses in mouse vas deferens and its relation to calcium. 858 51

Acute and chronic effects of elevated extracellular concentrations of potassium ions ([K+]0) and/or noradrenaline were studied in homogenates of primary cultures of mouse astrocytes, from the cerebral cortex or the spinal cord, and of primary cultures of mouse cerebral cortical neurons. NA+, K+-ATPase activity in cerebral cortical astrocytes showed a Km value of 1.9 mM with confidence limits of 1.3-2.9 mM and a Vmax of 5.4 mumol/h/mg protein with confidence limits of 3.3-8.1 mumol/h/mg protein. Due to the high Km value, the activity of the enzyme was significantly increased by an increase in [K+]0 in the interval 5-12 mM. In cerebral cortical neurons, Vmax was lower (1.77 +/- 0.06 mumol/h/mg protein) but the affinity was higher (Km 0.43 +/- 0.8 mM). With these kinetics, there is no stimulation of enzyme activity when [K+]0 is increased beyond control levels. In spinal cord astrocytes, the relative effect of increasing [K+]0 above 6 mM was larger than in cerebral astrocytes but the absolute activity of the enzyme was lower. Na+, K+-ATPase activity in both types of astrocyte was stimulated by noradrenaline and its beta-adrenergic subtype agonist isoproterenol but mainly or exclusively at 6 mM [K+]0. Noradrenaline also caused a stimulation in cortical neurons, but at non-physiological K+ concentrations this stimulation was converted to an inhibition, and isoproterenol had no stimulatory effect. Chronic exposure of cerebral cortical astrocytes to elevated [K+]0 caused a decrease in Na+, K+-ATPase activity when enzyme activity in the cells was subsequently measured at normal [K+]0. During exposure to 30 mM [K+]0 this "down-regulation" took place within 10 min. Conversely, chronic exposure to reduced [K+]0 led to an increase in Na+, K+-ATPase activity. Chronic exposure to noradrenaline had no significant effect but there was a tendency towards an increase.
 ...
PMID:Acute and chronic effects of potassium and noradrenaline on Na+, K+-ATPase activity in cultured mouse neurons and astrocytes. 881 52

Norepinephrine and epinephrine stimulate alpha- and beta-adrenergic receptors which, in turn, modulate force of contraction in heart muscle cells. However, chronic stimulation may be associated with growth-promoting effects and modulation of the cardiac phenotype. Sympathetic tone is chronically enhanced in chronic heart failure and results in a selective down regulation of beta 1 adrenergic receptors, most likely due to local mechanisms. Beyond reduced beta 1 receptor density and increased levels of inhibitory Gi proteins, there is now evidence that NO can modulate the beta-adrenergic stimulation in the human myocardium. Increased NO activity generated by an inducible NO synthase is associated with a reduced positive inotropic response to beta-agonists, a mechanism which may play an important role in inflammatory states such as myocarditis or sepsis. Experimental data suggests that stimulation of alpha-adrenergic receptors of cardiomyocytes results in cardiac growth and changes in phenotype which, in turn, may affect the functional properties of the myocardium. For example, phenylephrine can upregulate the expression of the sodium/calcium exchanger, while the expression SR Ca2+ ATPase may be reduced. The latter is also affected by angiotensin II. Similar changes in the expression of these crucial proteins for the cardiac calcium homeostasis have been reported in the failing human heart, raising the possibility that the increased sympathetic tone and the activated renin-angiotensin system may be involved in these changes.
 ...
PMID:[Sympathetic nervous system in heart failure: effect of catecholamines and nitric oxide]. 906 72

We have examined the ryanodine receptor, Ca(2+)-ATPase, calsequestrin and phospholamban mRNA levels in the left ventricles of pacing-induced heart failure and norepinephrine infusion dogs. The heart failure dogs showed a decrease in the levels of ryanodine receptor and Ca(2+)-ATPase mRNAs. Norepinephrine infusion caused a reduction of Ca(2+)-ATPase mRNA but no change in ryanodine receptor mRNA. There was a corresponding reduction of the immunoreactive Ca(2+)-ATPase protein levels in both heart failure and norepinephrine infusion animals compared to controls. In contrast, the mRNAs of calsequestrin and phospholamban were unchanged in dogs with either congestive heart failure or norepinephrine infusion. Thus, since norepinephrine infusion and congestive heart failure produced similar reductions of Ca(2+)-ATPase mRNA and protein, we postulate that the down-regulation of Ca(2+)-ATPase in congestive heart failure may be caused, at least in part, by sympathetic stimulation that occurs in heart failure.
 ...
PMID:Altered sarcoplasmic reticulum Ca2+ ATPase gene expression in congestive heart failure: effect of chronic norepinephrine infusion. 950 Aug 74

Renal sympathetic nerves play a central role in the regulation of tubular Na+ reabsorption. Norepinephrine (NE) and neuropeptide Y (NPY) are colocalized in renal sympathetic nerve endings. The purpose of this study is to examine the integrated effects of these neurotransmitters on the regulation of Na+-K+-ATPase, the enzyme responsible for active Na+ reabsorption in renal tubular cells. Studies were performed on proximal tubular segments, which express adrenergic alpha- and beta-receptors, as well as NPY-Y2 receptors. It was found that alpha- and beta-adrenergic agonists had opposing effects on Na+-K+-ATPase activity. beta-Adrenergic agonists induced a dose-dependent inhibition of the Na+-K+-ATPase activity, whereas alpha-adrenergic agonists stimulated the enzyme. NPY abolished beta-agonist-induced deactivation of Na+-K+-ATPase and enhanced alpha-agonist-induced activation of Na+-K+-ATPase. The beta-adrenergic agonist appeared to inhibit Na+-K+-ATPase activity via a cAMP pathway. NPY antagonized beta-agonist-induced accumulation of cAMP. In our preparation, NE alone had no net effect but stimulated the Na+-K+-ATPase activity in the presence of beta-adrenergic antagonists, as well as in the presence of NPY. The results indicate that, in renal tissue, NPY determines the net effect of its colocalized transmitter, NE, by its ability to attenuate the beta- and enhance the alpha-adrenergic effect.
 ...
PMID:Neuropeptide Y shifts equilibrium between alpha- and beta-adrenergic tonus in proximal tubule cells. 968 98

Recent findings have clarified the mechanisms regulating the night- and pineal-specific transcription of serotonin N-acetyltransferase, the rate-limiting enzyme in melatonin formation. Norepinephrine, acting via beta-adrenoceptors and cAMP at night, stimulates the cAMP response element binding protein, which turns on the transcription of N-acetyltransferase and inducible cAMP early repressor, the major inhibitor of N-acetyltransferase transcription. The tissue-specific gene expression within the pineal gland and retina derives, in part, from a pineal/retina-specific transcription factor, cone-rod homeobox protein, which binds to a pineal regulatory element. This regulatory element is present in promoters of pineal-selective enzymes, such as N-acetyltransferase, hydroxyindole-O-methyl transferase, and pineal night-specific ATPase.
 ...
PMID:Molecular rhythms in the pineal gland. 981 31

The present study examined renal dopaminergic activity and its response to high salt (HS) intake in adult (6-month-old) and old (24-month-old) Fischer 344 rats. Daily urinary excretion of L-3, 4-dihydroxyphenylalanine (L-DOPA), dopamine, and its metabolites 3, 4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid was similar in adult and old rats; by contrast, daily urinary excretion of norepinephrine in old rats was almost twice that in adult animals. HS intake (1% NaCl) over a period of 24 hours resulted in a 2-fold increase in the urinary excretion of dopamine, DOPAC, and norepinephrine in adult animals but not in old animals. Norepinephrine and L-DOPA plasma levels did not change during HS intake and were similar in both groups of rats. The natriuretic response to an HS intake in old rats (from 4.7+/-0.4 to 10.7+/-2.0 nmol. kg(-1). d(-1); Delta=6.0+/-0.9 nmol. kg(-1). d(-1)) was less than in adult rats (from 5.2+/-0.4 to 13.5+/-2.5 nmol. kg(-1). d(-1); Delta=8.3+/-0.8 nmol. kg(-1). d(-1)). A diuretic response to HS intake was observed in adult rats (from 20.9+/-2.3 to 37.6+/-2.8 mL. kg(-1). d(-1)) but not in old rats (from 37.7+/-5.7 to 42.3+/-6. 0 mL. kg(-1). d(-1)). Dopamine levels and dopamine/L-DOPA ratios in the renal cortex of old rats were greater than in adult rats. HS intake increased both dopamine levels and dopamine/L-DOPA ratios in the renal cortex of adult rats but not in old rats. Aromatic L-amino acid decarboxylase activity was higher in old rats than in adult rats; HS intake increased L-amino acid decarboxylase activity (nmol. mg protein(-1). l5 min(-1)) in adult rats (from 67+/-1 to 93+/-1) but not in old rats (from 86+/-2 to 87+/-2). Dopamine inhibited Na(+),K(+)-ATPase activity in proximal tubules obtained from adult rats, but it failed to exert such an inhibitory effect in old rats. It is concluded that renal dopaminergic tonus in old rats is higher than in adult rats but fails to respond to HS intake as observed in adult rats. This may be due in part to the inability of dopamine to inhibit Na(+),K(+)-ATPase activity in old rats.
 ...
PMID:Aging, high salt intake, and renal dopaminergic activity in Fischer 344 rats. 1052 44

The functional properties of the endothelium of human thyroid arteries remain unexplored. We investigated the intervention of nitric oxide (NO), prostacyclin (PGI(2)) and endothelium-derived hyperpolarizing factor (EDHF) in the responses to acetylcholine and noradrenaline in isolated thyroid arteries obtained from multi-organ donors. Artery rings were suspended in organ baths for isometric recording of tension. The contribution of NO, PGI(2) and EDHF to endothelium-dependent relaxation was determined by the inhibitory effects of N(G)-monomethyl-L-arginine (L-NMMA), indomethacin, and K(+) channel inhibitors respectively. Acetylcholine induced concentration-dependent relaxation; this effect was not modified by indomethacin and was only partly reduced by L-NMMA, but was abolished in endothelium-denuded rings. The relaxation resistant to indomethacin and L-NMMA was abolished by using either apamin combined with charybdotoxin, ouabain plus barium, or a high-K(+) solution. Noradrenaline induced concentration-dependent contractions which were of greater magnitude in arteries denuded of endothelium or in the presence of L-NMMA. In conclusion, the results indicate that in human thyroid arteries the endothelium significantly modulates responses to acetylcholine and noradrenaline through the release of NO and EDHF. EDHF plays a dominant role in acetylcholine-induced relaxation through activation of Ca(2+)-activated K(+) channels, inwardly rectifying K(+) channels and Na(+)-K(+)-ATPase.
 ...
PMID:Endothelium-dependent responses in human isolated thyroid arteries from donors. 1517 85

Human brain cortical homogenate derived from surgical operations exhibited Na(+), K(+)-ATPase and K-p-nitrophenylphosphatase activity values of 2.12 +/- 0.08 ?mol P(i)/mg protein/15 min and 0.38 +/- 0.01 ?mol p-nitrophenol/mg protein/15 min, respectively which is in the range of those observed in rat brain cortical homogenates. Vanadate concentration dependently inhibited the activity of both enzymes. Noradrenaline, dopamine and isoprenaline reversed the inhibitory effect of vanadate in the presence of EDTA (0.2 mM). When Mg(2+) concentration was enhanced from 4 to 24 mM, the inhibitory effect of vanadate (1 ?M) was significantly potentiated. Evidence has been obtained that the effect of catecholamines is not a receptor mediated process; antagnoists such as phentolamine, phenoxybenzamine, propranolol, haloperidol failed to prevent the effect of adrenoceptor agonists. It is concluded that there is an interaction between vanadate and noradrenaline on human brain Na, K-ATPase.
 ...
PMID:Effect of noradrenaline and vanadate on sodium, potassium-activated ATPase of human brain cortical homogenate. 2048 46

Norepinephrine (NE) is widely used to treat cardiac arrest and profound hypotension. A prolonged vasoconstriction of blood vessel could cause ischemia and hypoxia which results in a decrease in intracellular pH. V-ATPases pump protons across the plasma membranes of numerous cell types. V-ATPases-mediated intracellular regulation in the ischemic kidney is incompletely studied; we sought to determine the roles of V-ATPases in mice treated with NE causing vasoconstriction or acetylcholine causing vasodilatation to enable comparison of its relative contributions to the affected mice. Mice were divided into 5 groups. Histology and immunohistochemistry were performed to examine pathologic changes in nephron segments. The expression of V-ATPases B1, B2 subunits were examined by Q-PCR and western blotting correlated with the transcription and translation of V-ATPase. All NE treated mice exhibited pronounced renal tubular degradation. However, the tubular pathologies were reversed by ACh. In immunohistochemical studies, NE treated mice showed a higher density of staining in the collecting ducts. These changes were gradually diminished by the treatment with Ach after NE. In Q-PCR, V-ATPase B1 subunit showed a fair expression in all subsets. Western blotting analysis has shown V-ATPase B1 statistical significance in multiple groups treated by NE alone or ACh post to NE. The overdosage of norepinephrine in clinical treatment is harmful to the kidney by vasoconstriction caused hypoxia and acidosis. Our data demonstrated that acetylcholine as a vasodilating agent could aid the cells recovery from hypoxic condition. V-ATPase plays a role by removing H+ allowing cells to recover from cellular acidosis. These findings also help us understand the pathophysiology of renal tubular disorders.
 ...
PMID:Roles of vacuolar H+-ATPase in mice treated with norepinephrine and acetylcholine. 3266 66


<< Previous 1 2 3 4 5 6