Volume Maintenance in Isosmotic Conditions

Macknight, Anthony D. C.

doi:10.1016/s0070-2161(08)60366-4

Cited by 43 publications

(21 citation statements)

References 75 publications

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“…By comparing the readings of ion-selective electrodes with the values measured spectrophotometrically or by electron probe microanalysis, the activity coefficients were found to be 0.08/0.48 for Na ϩ and 1.2/0.67 for K ϩ in mature/ immature frog oocytes (113). Large deviations of ion activities from those in solution are not uncommon in cells (55,79) and have been demonstrated even in cell-free systems (123). Activity coefficients larger than unity likely indicate a decrease in the amount of solvent water (24).…”

Section: Osmotically Inactive Volumementioning

confidence: 99%

Possible causes of apoptotic volume decrease: an attempt at quantitative review

Model

2014

American Journal of Physiology-Cell Physiology

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Model MA. Possible causes of apoptotic volume decrease: an attempt at quantitative review. Am J Physiol Cell Physiol 306: C417-C424, 2014. First published November 6, 2013; doi:10.1152/ajpcell.00328.2013.-Cell shrinkage and dehydration are essential characteristics of apoptosis, and loss of as much as half of the initial cell volume is not uncommon. This phenomenon is usually explained by efflux of K ϩ and Cl Ϫ . We reexamine this hypothesis on the basis of the available data for ion concentrations and the requirements for osmotic equilibrium and electroneutrality. In addition to ion loss, we discuss the possible impacts of several other processes: efflux of low-molecular-weight osmolytes, acidification of the cytosol, effects of water channels and pumps, heterogeneity of intracellular water, and dissociation of apoptotic bodies. We conclude that most mammalian cells are theoretically capable of reducing their volume by 15-20% through ion loss or a decrease in cytosolic pH, although, in reality, the contribution of these mechanisms to apoptotic shrinkage may be smaller. Transitions between osmotically active and inactive water pools might influence cell volume as well; these mechanisms are poorly understood but are amenable to experimental study. Dissociation of apoptotic bodies is a separate mechanism of volume reduction and should be monitored closely; this can be best achieved by measurement of intracellular water, rather than cell volume. cell volume regulation; apoptosis; apoptotic volume decrease; intracellular water CELL SHRINKAGE is one the most reproducible signs of apoptosis (33,103). It has at least three distinct aspects: 1) weakening of the substrate attachment, resulting in cell rounding and reduced spreading, 2) dissociation of cell fragments known as apoptotic bodies, and 3) loss of intracellular water. Apoptotic body formation and the loss of water bring about a decrease in total cell volume. Volume changes in apoptotic cells have been measured by various techniques, and shrinkage by as much as 40 -85% has been reported (11,16,34,53,76,90). Shrinkage due to dehydration has received the most attention in the literature and is sometimes referred to as "apoptotic volume decrease" (AVD).The place of AVD in the sequence of apoptotic events and its significance for the rest of apoptosis have been addressed in numerous research papers and reviews (46,70,71,92,94). Apparently, AVD can be an early (5,8,15,28,34,49,53,81) or a late (26,60,85,90,117) response, depending on the particular system. A few exceptions to the rule that AVD must accompany apoptosis have also been described (11,13,56,65,121,127); nevertheless, it appears that, in the vast majority of apoptotic models, AVD does occur sooner or later.It has been hypothesized that the main purpose of AVD is to facilitate detachment of apoptotic bodies (91) or to oppose cell swelling and rupture that might develop otherwise (128). Although the definitive answer to this question is lacking, there can be little doubt that such a highly conserved property...

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Section: Osmotically Inactive Volumementioning

confidence: 99%

Possible causes of apoptotic volume decrease: an attempt at quantitative review

Model

2014

American Journal of Physiology-Cell Physiology

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“…By moving ions inward across the plasma membrane, Na+/K +/2C1-cotransport plays an important role in regulating cell volume in a number of tissues (Eveloff and Warnock, 1987;Larson and Spring, 1987;MacKnight, 1987;O'Grady, Palfrey, and Field, 1987;Hoffman and Simonsen, 1989). Na+/K+/2C1-cotransport has not been characterized fully in the heart.…”

Section: Introductionmentioning

confidence: 99%

Modulation of rabbit ventricular cell volume and Na+/K+/2Cl- cotransport by cGMP and atrial natriuretic factor.

Clemo

Feher

Baumgarten

1992

The Journal of General Physiology

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Previously we showed that atrial natriuretic factor (ANF) decreases cardiac cell volume by inhibiting ion uptake by Na+/K+/2CI-cotransport. Digital video microscopy was used to study the role of guanosine 3',5'-monophosphate (cGMP) in this process in rabbit ventricular myocytes. Each cell served as its own control, and relative cell volumes (volumetest/volumeco,trol) were determined. Exposure to 10 IxM 8-bromo-cGMP (8-Br-cGMP) reversibly decreased cell volume to 0.892 -0.007; the EDs0 was 0.77 +-0.33 tzM. Activating guanylate cyclase with 100 IxM sodium nitroprusside also decreased cell volume to 0.889 ---0.009. In contrast, 8-bromo-adenosine 3',5'-monophosphate (8-Br-AMP; 0.01-100 tzM) neither altered cell volume directly nor modified the response to 8-Br-cGMP. The idea that cGMP decreases cell volume by inhibiting Na+/K+/2C1-cotransport was tested by blocking the cotransporter with 10 I~M bumetanide (BUM) and removing the transported ions. After BUM treatment, 10 IxM 8-Br-cGMP failed to decrease cell volume. Replacement of Na ÷ with N-methyl-D-glucamine or C1-with methanesulfonate also prevented 8-Br-cGMP from shrinking cells. The data suggest that 8-Br-cGMP, like ANF, decreases ventricular cell volume by inhibiting Na+/K+/2C1-cotransport. Evidence that ANF modulates cell volume via cGMP was also obtained. Pretreatment with 10 IzM 8-Br-cGMP prevented the effect of 1 IzM ANF on cell volume, and ANF suppressed 8-Br-cGMP-induced cell shrinkage. Inhibiting guanylate cyclase with the quinolinedione LY83583 (10 tzM) diminished ANF-induced cell shrinkage, and inhibiting cGMP-specific phosphodiesterase with M&B22948 (Zaprihast; 100 IzM) amplified the volume decrease caused by a low dose of ANF (0.01 I~M) approximately fivefold. In contrast, neither 100 I~M 8-Br-cAMP nor 50 tzM forskolin affected the response to ANF. The effects of ANF, LY83583, and M&B29948 on cGMP levels in isolated ventricular myocytes were confirmed by 125I-cGMP radioimmunoassay. These data argue that ANF shrinks cardiac cells by increasing intracellular cGMP, thereby inhibiting Na+/K+/2C1-cotransport. Basal cGMP levels also appear to modulate cell volume.

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“…There is certainly evidence for a role of [Na-K]-ATPase in volume regulation [e.g.. Linshaw and Stapleton, 1978;Cooke and Macknight, 1984], It has been argued that the failure of some cells to increase in volume in media containing ouabain and the ability of swollen cells to restore their volume in such media reflect inadequate inhibition of this enzyme. Residual enzyme activity [Cooke, 1981;Macknight, 1981], possibly combined with alterations in the permeabilities of the pas sive pathways for diffusible ions [Macknight, 1987], would then explain the observations. Alternatively, it has been proposed that cells possess a contractile mechanism which regu lates volume by actively extruding isosmotic solution from the cells [Kleinzeller, 1965], that cytoplasmic vesicles take up ions and water which are then extruded from the cells by exocytosis [Van Rossum et al, 1987], and that there is a second sodium pump [Whittembury, 1968;Marin et al, 1985], We will consider some additional aspects of this ques tion later.…”

Section: Double-donnan or Pump-leak Hypothesismentioning

confidence: 99%

“…Typical values for cells in rabbit renal cortical slices incubated in isosmotic balanced sodium chloride medium. Major contributions come from non-diffusible cell osmoles (■), the Na and K which act as counterions for the net negative charge on these osmoles ( Hi), and cell chloride with its diffusible coun terions (additional Na+K) (¡Ü), [constructed from data in table 5, Macknight, 1987). cellular sodium content and, therefore, for the associated water content.…”

Section: Ion Conductance Pathwaysmentioning

confidence: 99%

Principles of Cell Volume Regulation

Macknight¹

1988

Kidney Blood Press Res

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Cell volume is determined by the content of osmotically active solute (cell osmoles) and the osmolarity of the extracellular fluid. Cell osmoles consist of non-diffusible and diffusible solutes. A large fraction of the diffusible cation content balances negative charges on the non-diffusible solutes. The content of diffusible solutes is determined by the electrochemical gradients driving them across the plasma membrane and the availability and activity of transport pathways in the membrane. The classical view that the sodium pump offsets passive leaks must be modified to accomodate the contributions of a number of secondary active transport processes, as well as to allow for changes in cell nondiffusible osmoles and in their net negative charge. The behaviour of cells in anisosmotic media is often different from that predicted for a perfect osmometer. In many cases this is a consequence of changes in cell osmole content. However, caution is required in extrapolating from in vitro responses of isolated cells to large, acutely induced changes in medium osmolality to the responses of tissues in vivo to more subtle changes in extracellular osmolality.

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Volume Maintenance in Isosmotic Conditions

Cited by 43 publications

References 75 publications

Possible causes of apoptotic volume decrease: an attempt at quantitative review

Possible causes of apoptotic volume decrease: an attempt at quantitative review

Modulation of rabbit ventricular cell volume and Na+/K+/2Cl- cotransport by cGMP and atrial natriuretic factor.

Principles of Cell Volume Regulation

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