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1.
Summary It has been shown experimentally that two different potentials appear across an intra-nonpermutating membrane3 when two different solutions (e.g., solution I: 0.1n NaCl+0.0001n KCl; and, solution II: 0.1n KCl + 0.0001n NaCl) are separated by such a membrane, and when the pores of the intra-nonpermutating membrane are supplied with ions from either solution I or solution II (in this case: essentially with Na+ ions from solution I, or essentially with K+ ions from solution II). The theoretical background, and other considerations, for these experiments will be found in reference.  相似文献   

2.
Summary With a suitable modification of the Farquhar and Palade technique the Na++K+-ATPase activity in guineapig thyroid is demonstrated. The addition of c-AMP (5×10–6 M or 1.5×10–5 M) to the incubation media produced an apparent intensification of the Na++K+-ATPase activity in the thyroid.This work was supported by a grant from ZMNU of Serbia.  相似文献   

3.
Treatment with the co-transport inhibitor, furosemide decreased36Cl flux across perfused Malpighian tubules ofLocusta. However, exclusion of36Cl from the bathing medium had not effect on22Na+ flux whereas substitution of bathing medium Na+ by K+ increased36Cl flux. Diuretic extract of corpora cardiaca increased22Na+ (by 106%) and36Cl (by 335%) fluxes differentially.  相似文献   

4.
Summary The volume regulation process at work in rabbit kidney cortex slices submitted to hypo-osmotic media show both a swelling limitation and a volume readjustment phase. Swelling limitation is Na+ dependent and is blocked by ouabain 10–3 M. There is, however, no need to implicate the activity of a ouabain sensitive Na+/K+ pump in this process.This work has been aided by a grant 1.5.422.82F from the FNRS to R.G. We wish to thank Mr J.M. Theate for his skilful assitance.  相似文献   

5.
Summary (Na++K+)-ATPase activity was higher in preparations from the ileum ofGlossina mortisans than in those from the rectum. This result suggests that the ileum as well as the rectum, may play a role in osmoregulation in the tsetse fly.  相似文献   

6.
Zusammenfassung Vorbehandlung von Arterienstreifen mit g-Strophantin (>10–8 g/ml) kehrt die mechanische Reaktion auf K+-Änderungen im Bereich von 1 bis 10 mM KCl, nicht aber die K+-Wirkung auf die Kontraktion durch Noradrenalin oder Barium um. Danach könnte die K+-Dilatation der Arterien auf der Aktivierung einer elektrogenen Na+-Pumpe beruhen.

The authors gratefully acknowledge the technical assistance by Mrs.B. Heinemann.  相似文献   

7.
Increasing evidence demonstrates that Na+, K+-ATPase plays an important role in pulmonary inflammation, but the mechanism remains largely unknown. In this study, we used cardiotonic steroids as Na+, K+-ATPase inhibitors to explore the possible involvement of Na+, K+-ATPase in pulmonary epithelial inflammation. The results demonstrated that mice after ouabain inhalation developed cyclooxygenase-2-dependent acute lung inflammation. The in vitro experiments further confirmed that Na+, K+-ATPase inhibitors significantly stimulated cyclooxygenase-2 expression in lung epithelial cells of human or murine origin, the process of which was participated by multiple cis-elements and trans-acting factors. Most importantly, we first described here that Na+, K+-ATPase inhibitors could evoke a significant Hu antigen R nuclear export in lung epithelial cells, which stabilized cyclooxygenase-2 mRNA by binding with a proximal AU-rich element within its 3′-untranslated region. In conclusion, HuR-mediated mRNA stabilization opens new avenues in understanding the importance of Na+, K+-ATPase, as well as its inhibitors in inflammation.  相似文献   

8.
Summary Na+, K+-ATPase inhibitors extracted from plasma of healthy human subjects displaced3H-ouabain binding to human erythrocytes and inhibited the Na+ efflux catalyzed by the Na+, K+-pump and unexpectedly the Na+, K+-cotransport system without alteration of the Na+, Na+-exchange or the Na+ passive permeability. This suggests the presence in healthy human plasma of endogenous factors with ouabain-like and furosemide-like activities.Acknowledgments. We are indebted to Dr M. A. Devynck for her advice on chemical measurements and to Dr R. P. Garay for his help with flux measurements  相似文献   

9.
Summary The forward motility of the rat caudal epididymal spermatozoa has been studied in different Na+ concentrations. When spermatozoa were suspended in a completely Na+-free solution, the forward motility suffered a progressive fall and after 3 h was completely suppressed. This effect was fully reversible on resuspending the spermatozoa in a solution containing Na+. Amiloride caused a fall in motility and the effect was similar to that of Na+ removal. The inhibition by amiloride of the motility was concentration dependent and the dose response curve showed an IC50-value of about 5×10–5 M. The role of Na+ influx in the maintenance of sperm motility was discussed.This work was supported by the World Health Organization.The technical assistance of Mr C.M. Li and the gift of amiloride from Merck, Sharp and Dohme are gratefully acknowledged.  相似文献   

10.
Summary In the isolated urinary bladder of the toad, 10–5–10–4M orthovanadate produces inhibition of the active transport of Na+ and H+ ions as well as of antidiuretic hormone-mediated osmotic flow of water. Since transport of H+ ions and osmotic water flow are not inhibited when (Na++K+)-ATPase is inhibited by ouabain, biological actions of vanadate are not necessarily related to inhibition of (Na++K+)-ATPase.This research was supported by grant AM-14915 from the National Institutes of Helath.  相似文献   

11.
Summary The effect of adrenaline on the Na+-pump in bullfrog (Rana catesbeiana) sympathetic ganglion cells was studied by use of electrophysiological methods. The rate of removal of excess Na+ injected into a ganglion cell was increased by adrenaline. The K+-activated hyperpolarization of cell membrane, which might be produced by an electrogenic Na+-pump, was also increased by adrenaline. These results suggested that adrenaline was able to accelerate the Na+-pump, possibly the electrogenic Na+-pump.  相似文献   

12.
In the present study, we have examined the intestinal Na+ transport, through the Na+-H+ exchanger, in ileal brush-border membrane vesicles (BBMV) isolated from spontaneously hypertensive rats (SHR), and normotensive Wistar Kyoto (WKY) rats as a control group. Na+ uptake into ileal BBMV was stimulated in the presence of a proton gradient (pH 5.5 inside/pH 7.5 outside) in SHR and WKY rats, resulting in a transient accumulation (overshoot) in both groups of rats. No overshoot was observed in the absence of a pH gradient. The magnitude of the accumulation was significantly higher in SHR than in WKY rats. Uptake of Na+ at equilibrium was identical in the presence and the absence of a proton gradient and was not changed in SHR. The use of amiloride inhibited pH gradient-driven Na+ uptake in a dose-dependent manner with a Ki of 90 μM and 100 μM for SHR and WKY rats, respectively. The relationship between proton gradient-driven Na+ uptake and external Na+ concentration was saturable and conformed to Michaelis-Menten kinetics in both SHR and WKY rats. Lineweaver-Burk analysis of the pH gradient-driven Na+ uptake indicated values of Vmax that were significantly increased in SHR compared to WKY rats (11.4±0.55 nmol/mg/8 s vs. 4.96±0.78 nmol/mg/8 s for SHR and WKY rats, respectively). In contrast, similar Km values for Na+ were found between SHR and WKY rats (4.0±0.2 mM vs. 4.9±0.6 mM for SHR and WKY rats, respectively). These studies show derangement in ileal BBMV Na+ transport of SHR, which is characterized by increased Na+-H+ exchanger activity. Received 18 December 1996; received after revision 3 February 1997; accepted 7 February 1997  相似文献   

13.
Summary Araplysillins-I and-II, two novel dibromotyrosine derivatives, were isolated fromPsammaplysilla arabica and their structure was elucidated by spectroscopic methods. They proved to be inhibitors of Na+/K+ ATPase and to have antimicrobial activity.  相似文献   

14.
Activation of δ-opioid receptors (DOR) attenuates anoxic K+ leakage and protects cortical neurons from anoxic insults by inhibiting Na+ influx. It is unknown, however, which pathway(s) that mediates the Na+ influx is the target of DOR signal. In the present work, we found that, in the cortex, (1) DOR protection was largely dependent on the inhibition of anoxic Na+ influxes mediated by voltage-gated Na+ channels; (2) DOR activation inhibited Na+ influx mediated by ionotropic glutamate N-methyl-D-aspartate (NMDA) receptors, but not that by non-NMDA receptors, although both played a role in anoxic K+ derangement; and (3) DOR activation had little effect on Na+/Ca2+ exchanger-based response to anoxia. We conclude that DOR activation attenuates anoxic K+ derangement by restricting Na+ influx mediated by Na+ channels and NMDA receptors, and that non-NMDA receptors and Na+/Ca2+ exchangers, although involved in anoxic K+ derangement in certain degrees, are less likely the targets of DOR signal. Received 26 November 2008; received after revision 26 December 2008; accepted 13 January 2009  相似文献   

15.
Selective pharmacological Na+/H+ exchange (NHE) inhibitors were used to identify functional NHE isoforms in human small intestinal enterocytes (Caco-2) and to distinguish between direct and indirect effects on transport via the intestinal di/tripeptide transporter hPepT1. The relative potencies of these inhibitors to inhibit 22Na+ influx identifies NHE3 and NHE1 as the apical and basolateral NHE isoforms. The Na+-dependent (NHE3-sensitive) component of apical dipeptide ([14C] Gly-Sar) uptake was inhibited by the selective NHE inhibitors with the same order of potency observed for inhibition of apical 22Na+ uptake. However, 5-(N-ethyl-N-isopropyl) amiloride (EIPA) also reduced [14C]Gly-Sar uptake in the absence of Na+ and this inhibition was concentration and pH (maximal at pH 5.5) dependent. NHE3 inhibition by S1611 and S3226 modulates dipeptide uptake indirectly by reducing the transapical driving force (H+ electrochemical gradient). EIPA (at 100 μM) has similar effects, but at higher concentrations (>200 μM) also has direct inhibitory effects on hPepT1.Received 28 February 2005; received after revision 20 April 2005; accepted 20 May 2005  相似文献   

16.
Summary Chicken spinal cord adenosine triphosphatases (both Na+, K+ stimulated and ouabain insensitive) were inhibited by tri-o-tolyl phosphate (TOTP, a neurotoxic organophosphate which is not a cholinesterase inhibitor) and mevinphos (a non-neurotoxic compound but inhibitor of cholinesterases). The inhibition was concentration and time dependent, with an initial rapid drop in activity followed by a gradual exponential decline.  相似文献   

17.
Hypoxic/ischemic disruption of ionic homeostasis is a critical trigger of neuronal injury/death in the brain. There is, however, no promising strategy against such pathophysiologic change to protect the brain from hypoxic/ischemic injury. Here, we present a novel finding that activation of δ-opioid receptors (DOR) reduced anoxic Na+ influx in the mouse cortex, which was completely blocked by DOR antagonism with naltrindole. Furthermore, we co-expressed DOR and Na+ channels in Xenopus oocytes and showed that DOR expression and activation indeed play an inhibitory role in Na+ channel regulation by decreasing the amplitude of sodium currents and increasing activation threshold of Na+ channels. Our results suggest that DOR protects from anoxic disruption of Na+ homeostasis via Na+ channel regulation. These data may potentially have significant impacts on understanding the intrinsic mechanism of neuronal responses to stress and provide clues for better solutions of hypoxic/ischemic encephalopathy, and for the exploration of acupuncture mechanism since acupuncture activates opioid system.  相似文献   

18.
Summary In isolated perfused posterior gills ofE. sinensis acclimated to fresh water, NH 4 + may be used as a counter-ion for Na+ active transport. This Na+/NH 4 + coupled transport can, however, only account for a small part of the Na+ total active influx.Chargé de Recherches du FNRS-Acknowledgments. This work has been aided by a grant crédit aux chercheurs from the FNRS and by a grant No. 2.4511.76 from the FRFC.  相似文献   

19.
Summary Na+, K+-adenosinetriphosphatase (Na+, K+-ATPase) activity was decreased in liver plasma membranes from rats in which cholestasis had been induced by i.v. administration of sodium taurolithocholate (5 moles/100 g b. wt). Incubation of liver plasma membranes with taurolithocholate (10–1300 M) caused significant and dose dependent reductions of Na+, K+-ATPase activity at taurolithocholate concentrations above 100 M. These findings lend support to the hypothesis that cholestasis induced by monohydroxy bile acids is at least partially the result of an inhibition of hepatic Na+, K+-ATPase activity.This work was supported by the Swiss National Science Foundation.The authors thank Mr H. Sägesser and Miss B. Schütz for technical assistance.  相似文献   

20.
The Na+,K+-ATPase, or sodium pump, is well known for its role in ion transport across the plasma membrane of animal cells. It carries out the transport of Na+ ions out of the cell and of K+ ions into the cell and thus maintains electrolyte and fluid balance. In addition to the fundamental ion-pumping function of the Na+,K+-ATPase, recent work has suggested additional roles for Na+,K+-ATPase in signal transduction and biomembrane structure. Several signaling pathways have been found to involve Na+,K+-ATPase, which serves as a docking station for a fast-growing number of protein interaction partners. In this review, we focus on Na+,K+-ATPase as a signal transducer, but also briefly discuss other Na+,K+-ATPase protein–protein interactions, providing a comprehensive overview of the diverse signaling functions ascribed to this well-known enzyme.  相似文献   

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