Insulin resistance, hypertension and cellular ion transport systems

1992 ◽  
Vol 29 (3-4) ◽  
pp. 196-200 ◽  
Author(s):  
Anna Solini ◽  
Ralph A. DeFronzo
Keyword(s):  
Insulin Resistance ◽  
Ion Transport ◽  
Transport Systems

Band-Type Dissipative Structure in Ion Transport Systems with Cylindrical Shape

1984 ◽  
Vol 53 (11) ◽  
pp. 4070-4082 ◽  
Author(s):  
Kiyoshi Toko ◽  
Satoru Iiyama ◽  
Kaoru Yamafuji
Keyword(s):  
Ion Transport ◽  
Dissipative Structure ◽  
Transport Systems ◽  
Cylindrical Shape ◽  
Band Type

Responses of trout gill ion transport systems to acute acidosis

1976 ◽  
Vol 64 (2) ◽  
pp. 511-515
Author(s):  
T. H. Kerstetter ◽  
R. Mize
Keyword(s):  
Lactic Acid ◽  
Rainbow Trout ◽  
Ion Transport ◽  
Ion Uptake ◽  
Transport Systems ◽  
Ph Changes ◽  
Blood Ph ◽  
Slow Infusion ◽  
Trout Gill

The response of rainbow trout Na+ and Cl- uptake systems to acute acidosis was tested by slow infusion of lactic acid into anaesthetized animals. Depression of blood pH by 0–4 pH unit had no effect on influx rates for either ion, and we conclude that gill ion uptake systems do not respond rapidly to blood pH changes.

The effect of dihydroquercetin on active and passive ion transport systems in plant vacuolar membrane

2009 ◽  
Vol 36 (1) ◽  
pp. 1-5 ◽  
Author(s):  
V. N. Nurminsky ◽  
N. V. Ozolina ◽  
J. G. Sapega ◽  
A. O. Zheleznykh ◽  
E. V. Pradedova ◽  
...  
Keyword(s):  
Ion Transport ◽  
Vacuolar Membrane ◽  
Transport Systems

scholarly journals Ion Transport and Membrane Potential in CNS Myelinated Axons I. Normoxic Conditions

1997 ◽  
Vol 78 (4) ◽  
pp. 2086-2094 ◽  
Author(s):  
Lisa Leppanen ◽  
Peter K. Stys
Keyword(s):  
Membrane Potential ◽  
Optic Nerve ◽  
Ion Transport ◽  
Transport Systems ◽  
Resting Membrane Potential ◽  
High Dose ◽  
Myelinated Axons ◽  
Gap Technique ◽  
Influx Pathways ◽  
Dose Dependent

Leppanen, Lisa and Peter K. Stys. Ion transport and membrane potential in CNS myelinated axons. I. Normoxic conditions. J. Neurophysiol. 78: 2086–2094, 1997. Compound resting membrane potential was recorded by the grease gap technique during normoxic conditions (37°C) in rat optic nerve, a representative CNS myelinated tract. Mean potential was −47 ± 3 (SD) mV and remained stable for 2–3 h. Input impedance of a single optic nerve axon was calculated to be ≈5 GΩ. Contribution of the Na+ pump to resting axonal potential is estimated at −7 mV. Ouabain (10 μM to 10 mM) evoked a dose-dependent depolarization that was maximal at ≥1 mM, depolarizing the nerves to ∼35–40% of control after 60 min. Inhibiting energy metabolism (CN− and iodoacetate) during high-dose ouabain (1–10 mM) exposure caused an additional depolarization, suggesting additional ATP-dependent, ouabain-insensitive ion transport systems. Perfusion with zero-Na+ (choline substituted) caused a transient hyperpolarization, that was greater than with tetrodotoxin (TTX; 1 μM) alone, indicating both TTX-sensitive and -insensitive Na+ influx pathways in resting rat optic nerve axons. Resting probability (P)K:PNa is calculated at 20:1. In contrast to choline-substituted solution, Li+-substituted zero-Na+ perfusate caused a rapid depolarization due to Na+ pump inhibition and the ability of Li+ to permeate the Na+ channel. TTX reduced, but did not prevent, ouabain- or zero-Na+/Li+–induced depolarization. We conclude that the primary Na+ influx path in resting rat optic nerve axons is the TTX-sensitive Na+ channel, with evidence for additional TTX-insensitive routes permeable to Na+ and Li+. In addition, maintenance of membrane potential is critically dependent on continuous Na+ pump activity due to the relatively high exchange of Na+ (via the above mentioned routes) and K+ across the membrane of resting optic axons.

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