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Measurement of Transmembrane Potential in the Study Of Systemic Disease*
Published in Richard C. Niemtzow, Transmembrane Potentials and Characteristics of Immune and Tumor Cell, 2020
J. Hamilton Licht, Hardin Jones
The third problem with this technique is its insensitivity. An abnormality in any of the functional components of the cell membrane can alter the intracellular milieu only if other components fail to compensate. For example, amphotericin B causes increased passive potassium efflux from cells. Compensatory increases in sodium-potassium-ATPase activity prevents net loss of potassium from cells.3 In this instance, a major disturbance in membrane function might have been overlooked had these investigators only examined intracellular electrolyte concentrations.
The development of hypertension in transgenic rats, TGR (mREN2)27
Published in H. Saito, Y. Yamori, M. Minami, S.H. Parvez, New Advances in SHR Research –, 2020
Jörg Peters, Detlev Ganten, John J. Mullins
Interestingly, studies on intact lymphocytes revealed elevated cytosolic sodium in TGR (mREN2) 27, compared with Sprague Dawley rats (TGR: 31.7 vs SDR: 18.2 mmol/L; Tepel et al., 1994). Furthermore, this was associated with reduced activity of the sodium/potassium ATPase (Tepel et al., 1994). Increased cytosolic sodium concentrations have been found in human primary hypertension, and also in the spontaneously hypertensive rat model of hypertension. Increased cytosolic sodium is involved in the pathogenesis of hypertension via the subsequent elevation of intracellular calcium and hence, increased vasoconstriction.
SBA Answers and Explanations
Published in Vivian A. Elwell, Jonathan M. Fishman, Rajat Chowdhury, SBAs for the MRCS Part A, 2018
Vivian A. Elwell, Jonathan M. Fishman, Rajat Chowdhury
The resting membrane potential is dependent on the electrogenic sodium–potassium ATPase pump and the relative intracellular and extracellular concentrations of ions on each side of the nerve cell membrane, as well as their relative permeabilities across the membrane. This establishes both a concentration (chemical) gradient and an electrical gradient across the nerve cell membrane – an electrochemical gradient. The equilibrium potential for a given ion species depends on the ratio of the concentrations of the ion outside to that inside the cell (the Nernst potential or equation). The Goldman constant-field (or Goldman–Hodgkin–Katz) equation is a more general form of the Nernst equation which allows for different permeabilities. Resting nerve cell membranes are about 100 times more permeable to K+ ions than to Na+ ions.
Cardiovascular benefit of SGLT2 inhibitors
Published in Critical Reviews in Clinical Laboratory Sciences, 2022
The cell membrane, composed of hydrophobic lipids, is impermeable to glucose. Accordingly, glucose transport across cell membranes is mediated by two families of transporters [1]: glucose transporters (GLUT), which operate by facilitated diffusion, and SGLT, which actively transport glucose by coupling with sodium. In the kidney, the sodium-potassium ATPase pump in the proximal tubule cell utilizes ATP to send 3 sodium ions outward into the blood, while bringing 2 potassium ions inward. This movement in the proximal tubule cell produces a downhill sodium ion gradient from the outside to the inside. The SGLT proteins utilize the energy from this downhill sodium ion gradient to transport glucose across the apical membrane against an uphill glucose gradient [2]. Importantly, this process is saturable, leading to glycosuria when plasma glucose levels exceed 10.0–11.1 mmo/l (180–200 mg/dl), usually seen only in patients with uncontrolled diabetes mellitus [3]. Because of this, SGLT2 inhibitors do not cause hypoglycemia in those without diabetes mellitus, which is relevant to their use in patients without this diagnosis (Figure 1).
Evaluation of the Presence and Functional Importance of Nucleoside Transporters in Lacrimal Gland for Tear Disposition of Intravenously Injected Substrate in Rabbits
Published in Current Eye Research, 2021
Hanuman Prasad Sharma, Nabanita Halder, Sundararajan Baskar Singh, T. Velpandian
The tear film is the first layer of protection working as a barrier between the external environment and the eye. It consists of three layers: superficial 0.1 μm thick lipid layer secreted by Meibomian glands, approximately 7 μm thick middle aqueous layer and innermost 0.02–0.04 μm thick mucinous layer secreted by conjunctival goblet cells.1,2 Most of the volume of the tear (~95%) is produced by the exocrine lacrimal gland,2 which is situated within the orbit in a superior temporal location.3 The ionic content of tears is known to be secreted through ion transporters and sodium-potassium ATPase (Na+/K+/ATPase). These transporters have been identified in the lacrimal gland of rats4,5 and rabbits.6,7 Sodium-potassium ATPase is an energy-driven ion channel that requires ATP for the exchange of Na+ and K+ ions through cellular membrane.8 Moreover, ATP is also required for the activation of P2X3 and P2X7 (membrane ion channels) receptors in lacrimal gland to increase intracellular calcium Ca2+ that stimulate protein secretion in the tears.9,10 Nucleosides and nucleobases are the precursors for the synthesis of ATP.11 Furthermore, nucleoside adenosine has been reported to modulate its receptors in the rabbit’s lacrimal gland.12
Evaluation of sodium orthovanadate as a radioprotective agent under total-body irradiation and partial-body irradiation conditions in mice
Published in International Journal of Radiation Biology, 2021
Yuichi Nishiyama, Akinori Morita, Bing Wang, Takuma Sakai, Dwi Ramadhani, Hidetoshi Satoh, Kaoru Tanaka, Megumi Sasatani, Shintaro Ochi, Masahide Tominaga, Hitoshi Ikushima, Junji Ueno, Mitsuru Nenoi, Shin Aoki
Vanadate is also known to inactivate protein tyrosine phosphatases (PTPase) (Gordon 1991) and adenosine triphosphatases (ATPase) (Aureliano and Crans 2009). Our previous study compared antiapoptotic effect of vanadate in irradiated MOLT-4 cells with several PTPase inhibitors, and the results suggested that the suppression of radiation-induced MOLT-4 apoptosis of vanadate is not associated with its PTPase-inhibiting effect (Morita et al. 2006). Therefore, the inhibiting effect of vanadate may not a contributing factor to the lethalities of TBI and PBI. Sodium-potassium ATPase (Na+/K+-ATPase), transmembrane protein that is effectively inhibited by vanadate (Aureliano and Crans 2009; Jiang et al. 2018), plays a central role in water and glucose absorptions in the intestine. Lebrun et al. demonstrated the reduction of Na+/K+-ATPase activity in rats treated with 8 Gy-TBI (Lebrun et al. 1998), and loss of the activity could result in radiation malabsorptive diarrhea (MacNaughton 2000). Since weight gain, stool consistency, and survival rate showed no differences for 60 days between unirradiated mice treated with or without a single injection of 20 mg/kg vanadate (data not shown), the dose was considered to have no effect on physiological condition. Detailed studies are needed to examine the vanadate requirement sufficient to inactivate Na+/K+-ATPase in GI tissue and how the inactivation affect in the development of radiation GI syndrome.