Ionic basis for membrane potential changes induced by hypoosmotic stress in guinea-pig ventricular myocytes

Abstract

Initial prolongation followed by later shortening of APD in hypotonic solution are mostly caused by different sequences of NSC, I(Ks) and I(Clswell) currents activation. Depolarization of RP in hypotonic solution is probably due to dilution of subsarcolemmal K(+) concentration and/or change in permeability ratio for Na(+) and K(+).

The Effects of K+ Channels Modulators Terikalant and Glibenclamide on Membrane Potential Changes Induced by Hypotonic Challenge of Guinea Pig Ventricular Myocytes

“…However, the mechanism of depolarization of resting potential observed in all ventricular myocytes exposed to hypotonic solution was not elucidated. A possible participation of I K1 to the above-mentioned phenomenon was not completely excluded (4,7). In this study we measured whole cell currents at voltages slightly negative (-80 to -110 mV) or positive (-80 to -40 mV) in relation to the RP.…”

“…Most of those currents were identified as I Ks (slow component of delayed rectifier potassium current), I Cl,swell (swelling-induced chloride current), and I NSC (non-selective cation current) (4 -6). There have been also described typical membrane potential changes under such a condition: initial prolongation with a secondary shortening of APD and simultaneous depolarization of RP (7). However, the mechanism of depolarization of resting potential observed in all ventricular myocytes exposed to hypotonic solution was not elucidated.…”

“…On the other hand, Priebe and Beuckelmann reported that activation of I KATP current produced APD shortening in guinea pig ventricular myocytes during hypotonic stress (10). Hence, we undertook our experiments in order to find out whether activation of I KATP and I K1 currents contribute to APD shortening and RP depolarization of guinea pig ventricular myocytes treated by hypotonic solution, employing pharmacological tools and the patch clamp technique under the same experimental conditions as previously (7).…”

“…Two important events appearing during hypotonic stress of guinea pig ventricular myocytes, APD shortening and depolarization of RP, have not yet been explained in terms of ionic mechanisms. Activation of ATP-sensitive K + currents (I KATP ) and inward rectifier K + currents (I K1 ) could contribute to APD shortening and RP depolarization, respectively, but their roles in the above-mentioned phenomena have not been clarified (4,7,10). For instance, Du and Sorota (4) have shown that depolarization of resting potential during hypotonic challenge in canine atrial myocytes was due to activation *Corresponding author.…”

Trypanosoma brucei Vacuolar Transporter Chaperone 4 (TbVtc4) Is an Acidocalcisome Polyphosphate Kinase Required for in Vivo Infection

“…Regulatory Volume Changes under Osmotic Stress ConditionsFor osmotic stress under constant ionic strength, the following buffers described previously (37,38) with some modifications were used: isotonic (64 mM NaCl, 4 mM KCl, 1.8 mM CaCl 2 , 0.53 mM MgCl 2 , 5.5 mM glucose, 5 mM Na-Hepes, pH 7.4, and 150 mM mannitol; 320 Ϯ 5 mosM, as determined using an Advanced Instruments 3D3 osmometer), hypotonic (the same as isotonic but without mannitol; 160 Ϯ 5 mosM), and hypertonic (the same as isotonic but with increased mannitol concentration to 1.2 M; 980 Ϯ 5 mosM). Samples of 1 ϫ 10 7 BSF (single marker strain and TbVtc4-KO with or without tetracycline) were collected, washed with isotonic buffer prewarmed at 37°C, and resuspended in 100 l of isotonic buffer.…”