Cell swelling and ion transport pathways in cardiac myocytes

1996 ◽  
Vol 32 (1) ◽  
pp. 85-97 ◽  
Author(s):  
J VANDENBERG
Keyword(s):  
Ion Transport ◽  
Cardiac Myocytes ◽  
Cell Swelling ◽  
Transport Pathways

scholarly journals Cell swelling and ion transport pathways in cardiac myocytes

1996 ◽  
Vol 32 (1) ◽  
pp. 85-97 ◽  
Author(s):  
J. I. Vandenberg ◽  
S. A. Rees ◽  
A. R. Wright ◽  
T. Powell
Keyword(s):  
Ion Transport ◽  
Cardiac Myocytes ◽  
Cell Swelling ◽  
Transport Pathways

Cation transport and volume regulation in sickle red blood cells

1993 ◽  
Vol 264 (2) ◽  
pp. C251-C270 ◽  
Author(s):  
C. H. Joiner
Keyword(s):  
Sickle Cell ◽  
Vascular Occlusion ◽  
Cell Swelling ◽  
K Channel ◽  
Transport Pathways ◽  
Root Cause ◽  
Sickle Cells ◽  
Cellular Dehydration ◽  
Mechanism Of Dehydration

Cellular dehydration is one of several pathological features of the sickle cell. Cation depletion is quite severe in certain populations of sickle cells and contributes to the rheological dysfunction that is the root cause of vascular occlusion in this disease. The mechanism of dehydration of sickle cells in vivo has not been ascertained, but three transport pathways may play important roles in this process. These include the deoxygenation-induced pathway that permits passive K+ loss and entry of Na+ and Ca2+; the K(+)-Cl- cotransport pathway, activated by acidification or cell swelling; and the Ca(2+)-activated K+ channel, or Gardos pathway, presumably activated by deoxygenation-induced Ca2+ influx. Recent evidence suggests that these pathways may interact in vivo. Heterogeneity exists among sickle cells as to the rate at which they become dense, suggesting that other factors may affect the activity or interactions of these pathways. Understanding the mechanism of dehydration of sickle cells may provide opportunities for pharmacological manipulation of cell volume to mitigate some of the symptoms of sickle cell disease.

Abstract 99: Hypotonic Swelling Promotes Nitric Oxide Release in Cardiac Ventricular Myocytes

2014 ◽  
Vol 115 (suppl_1) ◽  
Author(s):  
Luis Gonano ◽  
Malena Morell ◽  
Juan I Burgos ◽  
Martin Vila Petroff
Keyword(s):  
Nitric Oxide ◽  
Cardiac Myocytes ◽  
Cardiac Myocyte ◽  
Contractile Function ◽  
Cell Swelling ◽  
Contractile Dysfunction ◽  
Ischemia And Reperfusion ◽  
Hypotonic Solution ◽  
No Release ◽  
Hypotonic Swelling

Cardiac myocyte swelling occurs in multiple pathological situations and in particular contributes to the deleterious effects of ischemia and reperfusion by promoting contractile dysfunction. We investigated whether hypotonic swelling promotes nitric oxide (NO) release in cardiac myocytes and if so, whether it impacts on swelling induced contractile dysfunction. Perfusing rat cardiac myocytes, loaded with the NO sensor DAF-FM, with a hypotonic solution (HS; 217 mOsm), increased cell volume, reduced myocyte contraction and Ca2+ transient amplitude and significantly increased DAF-FM fluorescence. When cells were exposed to the HS supplemented with 2.5 mM of the NO synthase inhibitor L-NAME, cell swelling occurred in the absence of NO release. Swelling-induced NO release was also prevented by the NOS1 inhibitor, Nitroguanidine. In addition, Colchicine (an inhibitor of microtubule polymerization) prevented the increase in DAF-FM fluorescence induced by HS indicating that microtubule integrity is necessary for swelling-induced NO release. The swelling-induced negative inotropic effect was exacerbated in the presence of either L-NAME, Nitroguandine or the guanylate cyclase inhibitor, ODQ, suggesting that NOS1-derived NO provides contractile support via a GMP-dependent mechanism. Indeed, ODQ reduced Ca2+ wave velocity and the HS-induced increment in ryanodine receptor (RyR2) phosphorylation at site Ser2808 suggesting that in the context of hypotonic swelling, cGMP may contribute to preserve contractile function by enhancing SR Ca2+ release. Our findings suggest a novel mechanism for NO release in cardiac myocytes with putative pathophysiological relevance in the context of ischemia and reperfusion, where it may be cardioprotective by reducing the extent of contractile dysfunction associated with hypotonic swelling.

Na+ and Cl- transport across rabbit nonciliated bronchiolar epithelial (Clara) cells

1989 ◽  
Vol 256 (4) ◽  
pp. C893-C901 ◽  
Author(s):  
M. R. Van Scott ◽  
C. W. Davis ◽  
R. C. Boucher
Keyword(s):  
Ion Transport ◽  
Short Circuit ◽  
Flux Ratio ◽  
Open Circuit ◽  
Clara Cell ◽  
Clara Cells ◽  
Transport Pathway ◽  
Transport Pathways ◽  
Serum Free ◽  
Significant Difference

Radioisotopic flux measurements were performed on rabbit Clara cell epithelium cultured in serum-free hormone-supplemented medium to identify the major ion transport pathways in the cell type. Clara cells cultured in serum-free hormone-supplemented medium exhibit a large short-circuit current compared with cells maintained in serum-containing medium (45 microA/cm2 vs. 15 microA/cm2). The responses to amiloride and isoproterenol, however, are similar for cells grown in the two media. A net amiloride-sensitive movement of Na+ in the mucosal (M)-to-serosal (S) direction undershort- and open-circuit conditions is detected (1.48 and 0.67 mueq.h-1.cm-2, respectively). No statistically significant difference in the unidirectional fluxes of Cl- is apparent in the basal state, but a net flux of Cl- in the S-to-M direction is observed after exposure of the apical membrane to amiloride (0.93 mueq.h-1.cm-2). The partial ionic conductances for Na+ and Cl- estimated from the fluxes measured in the passive directions (JNaS----M, JClM----S) exceed the total tissue conductance by 20%. Ussing flux ratio analyses of Cl- movements at clamped potentials between -60 and +20 mV show that Cl- movements are not strictly through passive conductive pathways at negative potentials. The movement of Cl- can be modeled by passive diffusion combined with Cl- -Cl- exchange equal to 20% of total passive fluxes of Na+ and Cl-. These observations indicate that 1) Na+ absorption is the major active ion transport pathway across cultured Clara cells, 2) active Cl- secretion is minimal in the basal state, and 3) approximately 20% of the unidirectional Cl- fluxes occur via nonconductive pathways.

Effects of a short-chain phospholipid on ion transport pathways in rabbit nasal airway epithelium

1996 ◽  
Vol 271 (4) ◽  
pp. L646-L655 ◽  
Author(s):  
M. Ropke ◽  
M. Hansen ◽  
S. Carstens ◽  
P. Christensen ◽  
G. Danielsen ◽  
...  
Keyword(s):  
Ion Transport ◽  
Airway Epithelium ◽  
Short Circuit ◽  
Apical Cell ◽  
Short Chain ◽  
Nasal Airway ◽  
Na Channels ◽  
Transport Pathways ◽  
Lipoxygenase Inhibitors ◽  
Ussing Chambers

We investigated the mechanism of interference of mucosal application of the short-chain phospholipid didecanoyl-L-alpha-phosphatidylcholine (DDPC; 0.1-0.5%) with ion transport pathways in isolated rabbit nasal airway epithelium (RNAE). Transports of Na+ and Cl- were evaluated from tracer ion fluxes, short-circuit current (Isc), and epithelial conductance (Gt) under short-circuit conditions in Ussing chambers. DDPC rapidly and reversibly abolished net Na+ absorption, reduced control Isc (approximately 110 microA/cm2) by approximately 80%, and induced a small Cl secretion. Intracellular Ca2+ concentration ([Ca2+]i) increased dose dependently and transiently (measured by fura 2 in cultured rabbit airway epithelium), but ionomycin failed to mimic the decrease in Isc. The rise in [Ca2+]i may explain a Ba(2+)-sensitive transient activation of a basolateral K+ conductance. Indomethacin-sensitive prostaglandin E2 production in RNAE increased severalfold, but cyclooxygenase and lipoxygenase inhibitors did not prevent DDPC-induced changes in Isc. DDPC initially decreased control Gt (approximately 13 mS/cm2) by approximately 25% due to inhibition of amiloride-sensitive Na+ channels, and then reversibly increased Gt to approximately 45% above control values. Passive Na+ fluxes increased more than Cl fluxes, suggesting that the increase in Gt is due to formation of a paracellular shunt conductance in parallel with unaffected, anion-selective tight junction channels. The results suggest that DDPC inhibits apical membrane Na+ channels and causes structural changes in tight junctions after incorporation in apical cell membranes.

A safe and fast-charging lithium-ion battery anode using MXene supported Li3VO4

2019 ◽  
Vol 7 (18) ◽  
pp. 11250-11256 ◽  
Author(s):  
Yanghang Huang ◽  
Haochen Yang ◽  
Yi Zhang ◽  
Yamin Zhang ◽  
Yutong Wu ◽  
...  
Keyword(s):  
Ion Transport ◽  
Lithium Ion Battery ◽  
Anode Material ◽  
Three Dimensional ◽  
Lithium Ion ◽  
Ionic Transport ◽  
Transport Pathways ◽  
Fast Charging ◽  
Battery Anode

An innovative anode material of lithium-ion battery, Li3VO4/Ti3C2Tx, was synthesized. The overall three-dimensional electronic and ionic transport pathways were formed in anode, which promoted both electron and ion transport during the lithiation and delithiation processes.

Methylprednisolone increases absorptive capacity of rabbit ileum in vitro

1983 ◽  
Vol 245 (4) ◽  
pp. G562-G567 ◽  
Author(s):  
J. H. Sellin ◽  
R. C. DeSoignie
Keyword(s):  
Ion Transport ◽  
Absorptive Capacity ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Ion Flux ◽  
Rabbit Ileum ◽  
Transport Pathways ◽  
Na Pump ◽  
Intestinal Ion Transport

The effect of glucocorticoids on intestinal ion transport was studied in ileum in vitro from control and methylprednisolone (MP)-treated (40 mg im for 2 days) rabbits under the following conditions: a) basal rates of Na and Cl transport, b) the response to an individual absorptive stimulus (alanine, glucose, or epinephrine), and c) the response to a combination of the three absorptive stimuli. The results indicate that MP 1) increases basal absorption of Na and Cl and secretion of bicarbonate (as measured by residual ion flux), 2) does not alter the specific transport pathways stimulated by maximal doses of alanine, glucose, or epinephrine, but 3) significantly increases the absorptive capacity of ileum. After addition of combined alanine, glucose, and epinephrine, MP-treated ileum absorbed 15.8 mueq X cm-2 X h-1 Na (vs. 6.6 in controls, P less than 0.001) and 9.5 mueq X cm-2 X h-1 Cl (vs. 4.1 in controls, P less than 0.005). Additionally MP did not alter the Na dependence of either the short-circuit current or Cl absorption found in controls, although there appears to be a portion of residual ion flux insensitive to epinephrine inhibition. These data suggest that the MP-induced increase in absorptive capacity is due to an increase in a postapical transport step, most probably the Na pump.

Basolateral transport pathways for K+ and Cl- in rabbit proximal tubule: effects on cell volume

1991 ◽  
Vol 260 (1) ◽  
pp. F101-F109 ◽  
Author(s):  
L. Schild ◽  
P. S. Aronson ◽  
G. Giebisch
Keyword(s):  
Cell Volume ◽  
Basolateral Membrane ◽  
Cell Swelling ◽  
Volume Changes ◽  
Transport Pathways ◽  
Hypertonic Medium ◽  
Rate Of Increase ◽  
Kcl Transport ◽  
Cl Channels ◽  
Concentration Changes

To characterize the nature of K+ and Cl- transport pathways across basolateral membrane of rabbit proximal convoluted tubule, we used quantitative video microscopy to measure cell volume changes induced by rapid basolateral K+ and Cl- concentration changes. Elevating basolateral K+ resulted in cell swelling, which was largely inhibited by replacement of basolateral Cl- with cyclamate (85%) or by addition of 2 mM Ba2+ (72%). Substitution of basolateral Cl- by NO3- enhanced cell swelling, whereas substitution of Cl- by I- did not affect the K(+)-induced volume changes. Removal of Cl- from the bath reversed the cell swelling induced by raising K+ in the bath. Steady-state cell volume was 28% greater in hypotonic medium (250 mosmol/kgH2O) than in hypertonic medium (350 mosmol/kgH2O), and the rate of increase in cell volume induced by raising K+ was three times higher in hypotonic than in hypertonic medium. Substitution of Cl- by NO3- did not alter the effect of medium osmolality on K(+)-induced cell swelling, whereas addition of 0.2 mM diphenylamine-2-carboxylate inhibited the response (63%). We conclude that K(+)-induced cell swelling results from entry of K+ and Cl- into the cell across the basolateral membrane; it is proposed that transport of KCl across the basolateral cell membrane proceeds largely through two separate conductive pathways for K+ and Cl-. Cell swelling activates KCl transport occurring via K+ and Cl- channels across the basolateral membrane.

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