Cholinergic IPSP by Stimulation of the Electrogenic Sodium Pump

Nature ◽  
1969 ◽  
Vol 223 (5208) ◽  
pp. 864-865 ◽  
Author(s):  
G. A. KERKUT ◽  
L. C. BROWN ◽  
R. J. WALKER
1972 ◽  
Vol 50 (4) ◽  
pp. 378-380 ◽  
Author(s):  
Deepak Bose ◽  
Ian R. Innes

Ouabain or replacement of NaCl by LiCl abolishes the relaxation due to addition of KCl to sodium-rich cat carotid artery strips kept in a K+-free medium. Neither treatment antagonizes the relaxation due to β-adrenoceptor stimulation by l-isoprenaline. Unlike KCl-induced relaxation, the relaxation induced by l-isoprenaline is not due to stimulation of an electrogenic sodium pump.


Life Sciences ◽  
1969 ◽  
Vol 8 (5) ◽  
pp. 297-300 ◽  
Author(s):  
G.A. Kerkut ◽  
L.C. Brown ◽  
R.J. Walker

1977 ◽  
Vol 55 (4) ◽  
pp. 961-964 ◽  
Author(s):  
S. L. Lee ◽  
J. W. Phillis

The amines noradrenaline, dopamine, 5-hydroxytryptamine, and histamine (0.01–0.5 mM) enhanced the activity of Na-K-ATPase (EC 3.6.1.3) in rat cerebral cortical synaptosomal fractions. The activities of Mg-ATPase and Ca-Mg-ATPase were not significantly affected. No stimulation of Na-K-ATPase occurred in the presence of chelating agents (0.5 mM EGTA or EDTA) unless 0.5 mM calcium had also been added to the incubation medium. These results are consistent with the hypothesis that amines depress cerebral cortical neurones by activation of an electrogenic sodium pump. Calcium ions appear to be involved in this process.


Hypertension ◽  
1995 ◽  
Vol 26 (1) ◽  
pp. 177-185 ◽  
Author(s):  
Juliana Redondo ◽  
Concepción Peiró ◽  
Leocadio Rodríguez-Mañas ◽  
Mercedes Salaices ◽  
Jesús Marín ◽  
...  

1997 ◽  
Vol 200 (22) ◽  
pp. 2881-2892 ◽  
Author(s):  
P Leong ◽  
D Manahan

Early stages of animal development have high mass-specific rates of metabolism. The biochemical processes that establish metabolic rate and how these processes change during development are not understood. In this study, changes in Na+/K+-ATPase activity (the sodium pump) and rate of oxygen consumption were measured during embryonic and early larval development for two species of sea urchin, Strongylocentrotus purpuratus and Lytechinus pictus. Total (in vitro) Na+/K+-ATPase activity increased during development and could potentially account for up to 77 % of larval oxygen consumption in Strongylocentrotus purpuratus (pluteus stage) and 80 % in Lytechinus pictus (prism stage). The critical issue was addressed of what percentage of total enzyme activity is physiologically active in living embryos and larvae and thus what percentage of metabolism is established by the activity of the sodium pump during development. Early developmental stages of sea urchins are ideal for understanding the in vivo metabolic importance of Na+/K+-ATPase because of their small size and high permeability to radioactive tracers (86Rb+) added to sea water. A comparison of total and in vivo Na+/K+-ATPase activities revealed that approximately half of the total activity was utilized in vivo. The remainder represented a functionally active reserve that was subject to regulation, as verified by stimulation of in vivo Na+/K+-ATPase activity in the presence of the ionophore monensin. In the presence of monensin, in vivo Na+/K+-ATPase activities in embryos of S. purpuratus increased to 94 % of the maximum enzyme activity measured in vitro. Stimulation of in vivo Na+/K+-ATPase activity was also observed in the presence of dissolved alanine, presumably due to the requirement to remove the additional intracellular Na+ that was cotransported with alanine from sea water. The metabolic cost of maintaining the ionic balance was found to be high, with this process alone accounting for 40 % of the metabolic rate of sea urchin larvae (based on the measured fraction of total Na+/K+-ATPase that is physiologically active in larvae of S. purpuratus). Ontogenetic changes in pump activity and environmentally induced regulation of reserve Na+/K+-ATPase activity are important factors that determine a major proportion of the metabolic costs of sea urchin development.


1974 ◽  
Vol 73 (1) ◽  
pp. 156-160 ◽  
Author(s):  
Friedrich-Karl Pierau ◽  
Peter Torrey ◽  
David O. Carpenter

1969 ◽  
Vol 51 (1) ◽  
pp. 181-201
Author(s):  
R. B. MORETON

1. Sodium ions injected into giant neurones of Helix aspersa by diffusion from low-resistance microelectrodes caused hyperpolarization of the cells. Under these conditions the behaviour of the resting potential could be described by a modified ‘constant-field’ equation, including a term representing the effect of a potassiumsensitive, electrogenic sodium pump. 2. Exposure to potassium-free solution, ouabain or cyanide abolished the hyperpolarization, and caused a gradual fall in the intracellular potassium concentration, as estimated from the constant-field equation. 3. Assuming that this fall was due to replacement of intracellular potassium by injected sodium ions, it was possible to calculate the rates of injection and pumping of sodium ions, and, using the measured membrane resistance of the cell, the hyperpolarization which the sodium pump could cause, if it were electrogenic. 4. This was related to the observed hyperpolarization, supporting the view that the latter was caused by stimulation of the electrogenic sodium pump.


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