Is the Na+-Activated NADH-Quinone-Acceptor Oxidoreductase in Marine Bacteria and Moderate Halophiles a Primary Electrogenic Na+ Pump?

1991 ◽  
pp. 97-106 ◽  
Author(s):  
Robert A. MacLeod
Keyword(s):  
Marine Bacteria ◽  
Na Pump ◽  
Electrogenic Na Pump ◽  
Quinone Acceptor

Mechanisms underlying response to hypercapnia and bicarbonate of isolated dog cerebral arteries

1989 ◽  
Vol 257 (1) ◽  
pp. H141-H146 ◽  
Author(s):  
N. Toda ◽  
Y. Hatano ◽  
K. Mori
Keyword(s):  
Superoxide Dismutase ◽  
Cerebral Arteries ◽  
Extracellular Ph ◽  
Na Pump ◽  
Prostaglandin F2 Alpha ◽  
Electrogenic Na Pump ◽  
Cerebral Vasodilatation ◽  
High Level ◽  
Arterial Tone ◽  
Hcl Solution

In helical strips of dog cerebral arteries contracted with K+ or prostaglandin F2 alpha, the increase in CO2 from 5 to 15% in the gas aerating the bathing media produced a persistent relaxation in association with a rise of PCO2 and a fall of pH and PO2. Elevation of the NaHCO3 concentration from 25 to 75 mM in the bathing media under hypercapnia almost reversed the arterial tone when the osmolarity was balanced; the pH was completely reversed, whereas PCO2 was maintained at the high level. When 50 mM NaHCO3 were applied to the hypercapnic media without having the osmolarity balanced, the arteries relaxed further. Infusions of the HCl solution lowered the pH and relaxed the arterial strips; however, such a relaxation was significantly less than that caused by hypercapnia-induced acidosis. Relaxant responses to hypercapnia were attenuated by treatment with ouabain but were not influenced by amiloride and superoxide dismutase or by removal of endothelium. Relaxations due to hypertonic NaHCO3 were abolished or reversed to contractions by ouabain and were reduced by treatment with amiloride. It may be concluded that the hypercapnia-induced cerebroarterial relaxation is associated mainly with a fall of extracellular pH and is mediated partly by an activation of the electrogenic Na+ pump. Cerebral vasodilatation by increased osmolarity with NaHCO3 appears to result from stimulated Na+-H+ exchange and activated Na+ pump.

Mechanism underlying mannitol-induced relaxation in isolated monkey cerebral arteries

1992 ◽  
Vol 262 (3) ◽  
pp. H897-H902 ◽  
Author(s):  
N. Toda ◽  
K. Ayajiki ◽  
H. Toda ◽  
Y. Hatano ◽  
T. Okamura
Keyword(s):  
Superoxide Dismutase ◽  
Hydroxyl Radicals ◽  
Choline Chloride ◽  
Cerebral Arteries ◽  
Combined Treatment ◽  
The Other ◽  
Na Pump ◽  
Prostaglandin F2 Alpha ◽  
Arterial Contraction ◽  
Electrogenic Na Pump

The addition of mannitol (25, 50, and 100 mM) increased osmotic pressures of the bathing media from 293 to 317, 340 and 383 mosmol, respectively, and elicited a dose-related relaxation in monkey cerebral artery strips precontracted with K+ or prostaglandin F2 alpha. This relaxation was attenuated by ouabain, amiloride, catalase and oxyhemoglobin but was not influenced by superoxide dismutase and indomethacin. Combined treatment of the strips exposed to ouabain and amiloride with catalase produced an additional inhibition. H2O2 produced a contraction, which was abolished by catalase. Replacement of entire NaCl with choline chloride markedly suppressed the mannitol-induced relaxation. Relaxations caused by the addition of hypertonic NaHCO3 (25 and 50 mM) were also attenuated by ouabain and amiloride but were unaffected by catalase and oxyhemoglobin. It may be concluded that the mannitol-induced cerebroarterial relaxation is associated with an activation of the electrogenic Na+ pump and the Na(+)-H+ exchange and probably with scavenging of hydroxyl radicals responsible for the arterial contraction. On the other hand, hypertonic NaHCO3 relaxes monkey cerebral arteries, possibly due to an activation of the Na+ pump and the Na(+)-H+ exchange.

scholarly journals Properties of tetraethylammonium ion-resistant K+ channels in the photoreceptor membrane of the giant barnacle.

1981 ◽  
Vol 77 (6) ◽  
pp. 629-646 ◽  
Author(s):  
D R Edgington ◽  
A E Stuart
Keyword(s):  
Action Potential ◽  
Action Potentials ◽  
Cardiac Glycosides ◽  
Time Course ◽  
Photoreceptor Membrane ◽  
K Channels ◽  
Na Pump ◽  
Tetraethylammonium Ion ◽  
Electrogenic Na Pump ◽  
Time Courses

After the offset of illumination, barnacle photoreceptors undergo a large hyperpolarization that lasts seconds or minutes. We studied the mechanisms that generate this afterpotential by recording afterpotentials intracellularly from the medial photoreceptors of the giant barnacle Balanus nubilus. The afterpotential has two components with different time-courses: (a) an earlier component due to an increase in conductance to K+ that is not blocked by extracellular tetraethylammonium ion (TEA+) or 3-aminopyridine (3-AP) and (b) a later component that is sensitive to cardiac glycosides and that requires extracellular K+, suggesting that it is due to an electrogenic Na+ pump. The K+ conductance component increases in amplitude with increasing CA++ concentration and is inhibited by extracellular Co++; the Co++ inhibition can be overcome by increasing the Ca++ concentration. Thus, the K+ conductance component is Ca++ dependent. An afterpotential similar to that evoked by a brief flash of light is generated by depolarization with current in the dark and by eliciting Ca++ action potentials in the presence of TEA+ in the soma, axon, or terminal regions of the photoreceptor. The action potential undershoot is generated by an increase in conductance to K+ that is resistant to TEA+ and 3-AP and inhibited by Co++. The similarity in time-course and pharmacology of the hyperpolarization afterpotentials elicited by (a) a brief flash of light, (b) depolarization with current, and (c) an action potential indicates that Ca++-dependent K+ channels throughout the photoreceptor membrane are responsible for all three hyperpolarizing events.

scholarly journals Activation of Electrogenic Na+ Pump by Epinephrine in Bullfrog Atrium

1977 ◽  
Vol 18 (6) ◽  
pp. 860-866 ◽  
Author(s):  
Takashi AKASU ◽  
Yhukou OHTA ◽  
Kyozo KOKETSU
Keyword(s):  
Na Pump ◽  
Electrogenic Na Pump

Inhibition of the Electrogenic Na Pump Underlies Delayed Depolarization of Cortical Neurons After Mechanical Injury or Glutamate

1997 ◽  
Vol 77 (2) ◽  
pp. 632-638 ◽  
Author(s):  
Steven J. Tavalin ◽  
Earl F. Ellis ◽  
Leslie S. Satin
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Glutamate Receptor ◽  
Cortical Neurons ◽  
Superoxide Anion ◽  
Receptor Activation ◽  
Mechanical Injury ◽  
Electrophysiological Response ◽  
Na Pump ◽  
Electrogenic Na Pump

Tavalin, Steven J., Earl. F. Ellis, and Leslie S. Satin. Inhibition of the electrogenic Na pump underlies delayed depolarization of cortical neurons after mechanical injury or glutamate. J. Neurophysiol. 77: 632–638, 1997. We previously characterized the electrophysiological response of cortical neurons to a brief sublethal stretch-injury using an in vitro model of traumatic brain injury. This model revealed that cortical neurons undergo a stretch-induced delayed depolarization (SIDD) of their resting membrane potential (RMP) which is ∼10 mV in magnitude. SIDD is dependent on N-methyl-d-aspartate (NMDA) receptor activation, neuronal firing, and extracellular calcium for its induction but not its maintenance. SIDD was maximal 1 h after the insult and required incubation at 37°C. The present study examined the mechanism mediating SIDD and its relation to glutamate receptor activation. The Na pump inhibitor ouabain was used to assess the contribution of the Na pump to the RMP of control and stretched neurons using whole cell patch-clamp techniques. The nitric oxide (NO) synthase inhibitor Nω-nitro-L-arginine and a polyethylene glycol conjugate of superoxide dismutase were used to assess whether NO or superoxide anion, respectively, were involved in the induction of SIDD. Neurons were exposed to exogenous glutamate in the absence of cell stretch to determine whether glutamate alone can mimic SIDD. We report that SIDD is mediated by Na pump inhibition and is likely to result from reduced energy levels since the RMP of neurons dialyzed with a pipette solution containing 5 mM ATP were identical to controls. NO, but not superoxide anion, also may contribute to SIDD. A 3-min exposure to 10 μM glutamate produced a SIDD-like depolarization also associated with Na pump inhibition. The results suggest that Na pump inhibition secondary to alterations in cellular energetics underlies SIDD. Na pump inhibition due to glutamate exposure may contribute to traumatic brain injury or neurodegenerative diseases linked to glutamate receptor activation.

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