A chloride current associated with swelling of cultured chick heart cells.

Abstract

SUMMARY1. Cultured chick heart cells challenged by hyposmotic stress underwent regulatory volume decrease (RVD) that was attenuated by prior depletion of intracellular chloride.2. During hyposmotic swelling, cell aggregates experienced an initial increase in spontaneous contractile activity followed by eventual quiescence. Conventional microelectrode studies revealed an underlying increase in spontaneous electrical activity, followed by a sustained depolarization beyond threshold.3. Whole-cell patch clamp studies, with K+ currents blocked, indicated that exposure of cells to hyposmotic solution (NaCl reduction) resulted in a rapid osmotic swelling followed by a substantial increase in whole-cell conductance which persisted for the duration of hyposmotic exposure and was almost completely reversed on return to isosmotic bath solution.4. For a variety of Cl-concentrations, the reversal potentials (Erev) of the measured swelling-activated current closely followed the calculated Cl-equilibrium potential (Ecl) with a linear regression slope of

Chloride Channel Inhibition Blocks the Protection of Ischemic Preconditioning and Hypo-Osmotic Stress in Rabbit Ventricular Myocardium

“…31,32 We also determined the effect of IAA-94 (10 mol/L) and NPPB (1 mol/L) on PKC in an in vitro PKC activity assay as previously reported. 9 We found that IAA-94 and NPPB resulted in 94% and 96% retention of PKC activity, respectively. PKC inhibition by 10, 25, and 50 mol/L chelerythrine resulted in 55%, 40%, and 10% retention of PKC activity, respectively, whereas inhibition by 10 and 25 mol/L polymyxin B resulted in 16% and 0%, respectively, validating the assay.…”

“…5 Duan et al 6 have reported a tamoxifen-sensitive outwardly rectifying swell-activated Cl -current (I Cl,swell ) in rabbit atrial myocytes. I Cl,swell has also been reported in dog, 7,8 guinea pig, 7 chick, 9 and human 10 cardiomyocytes. Furthermore, I Cl,swell has been reported in a variety of noncardiac cells and demonstrates biophysical and pharmacological properties similar to those seen in cardiac myocytes.…”

Phorbol ester activation of chloride current in guinea‐pig ventricular myocytes

“…Cardiac I1c is stimulated by interventions that cause hyposmotic swelling (Tseng, 1992;Sorota, 1992;Zhang et al, 1993;Vandenberg et al, 1994;Shuba et al, 1996), protein kinase A (PKA) activation (Bahinski et al, 1989;Harvey & Hume, 1989;Ehara & Matsuura, 1993), and protein kinase C (PKC) activation (Walsh, 1991;Walsh & Long, 1994;Zhang et al, 1994). Of these, the regulation by PKC is the least well-characterized (for recent review, see Gadsby et al, 1995).…”

“…The movement of Cl-through sarcolemmal ion channels (Icl) in the heart influences the configuration of the action potential (Harvey et al, 1990;, participates in cell volume regulation (Tseng, 1992;Sorota, 1992;Zhang et al, 1993), and can promote arrhythmogenic activity (Ackerman & Clapham, 1993). Cardiac I1c is stimulated by interventions that cause hyposmotic swelling (Tseng, 1992;Sorota, 1992;Zhang et al, 1993;Vandenberg et al, 1994;Shuba et al, 1996), protein kinase A (PKA) activation (Bahinski et al, 1989;Harvey & Hume, 1989;Ehara & Matsuura, 1993), and protein kinase C (PKC) activation (Walsh, 1991;Walsh & Long, 1994;Zhang et al, 1994).…”

Swelling-induced chloride currents in neuroblastoma cells are calcium dependent

“…Initial studies with w-conotoxin MVIIC demonstrated inhibition of P-type channels in cerebellar Purkinje cells and CA1 hippocampal pyramidal cells (Hillgard et al, 1992). However, recent evidence (Wheeler et al, 1994;Zhang et al, 1994) suggests Q-and R-type Ca2+ channels may also be affected. Thus, w-conotoxin MVIIC-sensitive Ca2+ channels are activated in CHP-100 cells as a consequence of osmotic stress, but the exact identity of the channel subtype requires additional investigation.…”