scholarly journals Salinity change and cell volume: the response of tissues from the estuarine mussel Geukensia demissa.

1996 ◽  
Vol 199 (7) ◽  
pp. 1619-1630
Author(s):  
D S Neufeld ◽  
S H Wright

The response of cell volume to changes in external salinity was assessed in four tissues (gill, mantle, hemolymph cells and ventricle) of the estuarine mussel Geukensia demissa by using one or more of the following three indicators of cell volume response: changes in cell dimensions, cell water space and cell solute content. All three techniques indicated that short-term volume regulation was generally absent from gill tissue. Lateral cell height in gills, measured using differential interference contrast (DIC) microscopy, increased by approximately 20% after an abrupt exposure to reduced salinity (60% artificial sea water, ASW). There was significant variability in the observance of a regulatory volume decrease (RVD) subsequent to the initial swelling; cells remained swollen for 1 h after low-salinity exposure in two-thirds of the trials, while there was a return of cell volume towards control values in the remaining one-third of the trials. Lateral cell height increased linearly when salinity was gradually decreased from 100 to 60% ASW over 135 min. Cell height then returned to control values when the salinity was abruptly returned to 100% ASW, indicating that an RVD was not elicited by a slow change in salinity of the type normally encountered by estuarine mussels. Cumulative cell water space in gills increased by 47% after exposure to 60% ASW and the cells remained swollen for at least 4 h, returning to control values when gills were returned to 100% ASW. Consistent with the overall lack of an RVD, there was only a small decrease (approximately 5%) in cumulative osmolyte content (primarily taurine, betaine and K+) after 4 h in 60% ASW. Decreases in both cell water space and osmolyte content after 3 weeks of acclimation to 60% ASW indicated a long-term RVD of approximately 60%. Individual cells in the mantle epithelium also generally lacked an RVD in response to lowered salinity. Both abrupt and gradual decreases in salinity caused an increase in mantle cell height to a maximum of 25-30%, and cell height returned to the control height when salinity was abruptly returned to 100% ASW. Corresponding with the lack of an RVD in individual mantle cells, there was no change in solute content of the mantle tissue after 4 h of exposure to low salinity. The response of the volume of spherical hemolymph cells to 1 h of abrupt exposure to low salinity, calculated from measured cell diameters, likewise indicated that an RVD is generally lacking in these hemolymph cells. In the ventricle, however, there was a significant decrease in amino acid and betaine content after 4 h of exposure to low salinity, suggesting tissue-specific variability in the cellular response to salinity change. The consistent lack of a short-term RVD in many tissues may serve to avoid large energetic expenditures associated with repeated volume regulation in the face of the frequent, short-term changes in salinity encountered by estuarine mussels.

1996 ◽  
Vol 199 (2) ◽  
pp. 473-484 ◽  
Author(s):  
D S Neufeld ◽  
S H Wright

The response of gill cell volume in Mytilus californianus and Mytilus trossolus (=edulis) to acute changes in salinity was assessed using three independent indicators: optical measurement of lateral cell height, measurement of intracellular water content using radiolabeled tracers and measurement of the contents of the major osmolytes of the gills. Optical measurements indicated significant variation in the response of individual lateral cells of M. californianus to acute low-salinity shock. Lateral cell height increased by approximately 20% shortly after abrupt exposure to 60% artificial sea water (ASW). Following this initial swelling, we estimate that a substantial regulatory volume decrease (RVD) was present in 25% of the trials. More commonly, however, an RVD was either absent or minimal: cell height remained elevated for at least 1 h, then returned to the control height when gills were re-exposed to 100% ASW. Changes in the combined water space of all cells in the gill, measured as the difference between total water space and extracellular space ([14C]polyethylene glycol space), indicated that cell volume regulation in the gill as an organ was also absent or minimal. Cell water space was 2.16 ml g-1 dry mass in isolated gills of M. californianus acclimated to 100% sea water in the laboratory and increased to 2.83 ml g-1 dry mass after a 6 min exposure to 60% ASW. Cell water space was still 2.81 ml g-1 dry mass after 1 h in 60% ASW and returned to 2.06 ml g-1 dry mass upon re-exposure to 100% ASW. Consistent with these observations, the gill contents of the principal cytoplasmic osmolytes (taurine, betaine and K+) were unchanged (approximately 450, 250 and 230 mu mol g-1 dry mass, respectively) following exposure of gills from 100% ASW-acclimated mussels to 60% ASW. A decrease in cell water space to 2.66 ml g-1 dry mass after 4 weeks of acclimation to 60% ASW corresponded with a 37% decrease in betaine content; taurine and K+ contents were unchanged. The changes in water space and solute content of gills from freshly collected M. californianus and M. trossolus were also consistent with the absence of volume regulation; cell water space remained elevated for at least 1 h after low-salinity exposure, and solute contents were unchanged after this period. We calculated the potential energetic cost of cell volume regulation for mussels exposed to 12 h of sinusoidal fluctuations between 100% and 50% sea water; solute uptake for full volume regulation in all tissues would cost a minimum of approximately 30% of the standard metabolic rate during the period of salinity increase. The routine absence of substantial cell volume regulation in Mytilus gill may reflect the potentially high energetic cost of volume regulation in the face of the large and frequent salinity fluctuations that are regularly encountered by estuarine bivalves.


1998 ◽  
Vol 201 (9) ◽  
pp. 1421-1431 ◽  
Author(s):  
D Neufeld ◽  
S Wright

We acclimated the estuarine mussel Geukensia demissa to a regime of sinusoidal salinity cycling (12 h cycle between 100 % and 60 % seawater) and correlated changes in the volume of gill cells with changes in several indicators of the functional status of gill cells (rate of O2 consumption, ATP content and amino acid transport). There was no indication of short-term volume regulation in the gill cells of mussels acclimated to salinity cycling. When exposed to cycling salinity, cell water space consistently increased to approximately 3 ml g-1 dry mass during the cycle troughs (60 % seawater) and returned to approximately 2 ml g-1 dry mass at the cycle peaks (100 % seawater). In mussels acclimated for 2 weeks to cycling salinity, the gill contents of betaine, taurine and K+ were unchanged (approximately 240, 230 and 160 micromol g-1 dry mass, respectively) between the 60 % and 100 % seawater portions of the salinity cycle. The changes in cell volume did not appear to be associated with large perturbations in the functional status of cells. The rate of O2 consumption was approximately 100 microl O2 g-1 dry mass min-1, and ATP content was approximately 30 micromol g-1 protein, in all salinities to which mussels were exposed. Rates of uptake of taurine, leucine and phenylalanine decreased by approximately 50 % during the first sinusoidal decrease to 60 % seawater, but recovered following re-exposure to 100 % seawater. Uptake rates of all three amino acids were unaffected by any subsequent salinity cycles. These results suggest (1) that the regulation of gill cell volume is normally absent from mussels exposed to repeated, gradual salinity changes, and (2) that any effects of changes in cell volume are not severe enough to justify the energetic expenditure that would be associated with repeated regulation of cell volume. Unlike the response of gill cells to cycling salinity, there was a decrease in the solute contents of ventricles during the salinity troughs compared with the salinity peaks, suggesting that the presence of short-term volume regulation may be more critical in the ventricle.


1994 ◽  
Vol 267 (3) ◽  
pp. E343-E355 ◽  
Author(s):  
D. Haussinger ◽  
F. Lang ◽  
W. Gerok

Cellular hydration can change within minutes under the influence of hormones, nutrients, and oxidative stress. Such short-term modulation of cell volume within a narrow range acts per se as a potent signal which modifies cellular metabolism and gene expression. It appears that cell swelling and cell shrinkage lead to certain opposite patterns of cellular metabolic function. Apparently, hormones and amino acids can trigger those patterns simply by altering cell volume. Thus alterations of cellular hydration may represent another important mechanism for metabolic control and act as another second or third messenger linking cell function to hormonal and environmental alterations.


1979 ◽  
Vol 47 (5) ◽  
pp. 1031-1038 ◽  
Author(s):  
J. E. Greenleaf ◽  
V. A. Convertino ◽  
G. R. Mangseth

Our purpose was 1) to test the hypothesis that in man there is a range of plasma osmolality within which the red cell volume (RCV) and mean corpuscular volume (MCV) remain essentially constant and 2) to determine the upper limit of this range. During a variety of stresses--submaximal and maximal exercise, heat and altitude exposure, +Gz acceleration, and tilting--changes in plasma osmolality between -1 and +13 mosmol/kg resulted in essentially no change in the regression of percent change in plasma volume (PV) calculated from a change in hematocrit (Hct) on that calculated from a change in Hct + hemoglobin (Hb), i.e., the RCV and MCV were constant. Factors that do not influence RCV are the level of metabolism, heat exposure at rest, and short-term orthostasis (heat-to-foot acceleration). Factors that may influence RCV are exposure to high altitude and long-term orthostasis (head-up tilting). Factors that definitely influence RCV are prior dehydration and extended (greater than 2 h) periods of stress. Thus, either the Hct or the Hct + Hb equations can be used to calculate percent changes in PV under short-term (less than 2 h) periods of stress when the change in plasma osmolality is less than 13 mosmol/kg.


1994 ◽  
Vol 194 (1) ◽  
pp. 47-68
Author(s):  
A L Silva ◽  
S H Wright

Long-term acclimation of Mytilus californianus to 60% artificial sea water (585 mosmol l-1; ASW) led to a 30-40% decrease in the taurine (53.5-36.9 mumol g-1 wet mass) and betaine (44.8-26.2 mumol g-1 wet mass) content of gill tissue, compared with that of control animals held in 100% ASW (980 mosmol l-1). The K+ content of gills did not change following long-term acclimation to reduced salinity. In contrast, losses of all three solutes during a brief (60 min) exposure to 60% ASW were less than or equal to 15%. Nevertheless, the swelling of gill cells that occurred after acute exposure to 60% ASW was followed by a return towards the control volume. Direct optical measurement of single gill filaments confirmed that, during an acute exposure to reduced salinity, ciliated lateral cells increased in cell height (volume) and then underwent a regulatory volume decrease (RVD) with a half-time of approximately 10 min. This short-term RVD was completely inhibited by exposure to 1 mmol l-1 quinidine, a K+ channel blocker, but only when the drug was applied to the basolateral aspect of the gill epithelium. Application of 1 mumol l-1 valinomycin relieved the inhibition by quinidine of the gill RVD. However, addition of valinomycin did not accelerate the rate of RVD observed in the absence of quinidine. These results indicate that long-term acclimation of Mytilus californianus gill in dilute sea water involves primarily losses of taurine and betaine, whereas short-term regulation of cell volume may involve an electrically conductive loss of intracellular K+ and a counter ion.


1982 ◽  
Vol 243 (3) ◽  
pp. C140-C145 ◽  
Author(s):  
A. C. Ericson ◽  
K. R. Spring

NaCl entry into Necturus maculosus gallbladder epithelial cells was studied by determination of the rate of fluid movement into the cell when the Na+-K+-ATPase was inhibited by 10(-4) M ouabain in the serosal bathing solution. The cell swelling was due to continuing entrance of NaCl into the cell across the apical membrane, which increased the solute content of the cell; the resultant rise in cell osmolality induced water flow and cell swelling. The rate of swelling was 4.3% of the cell volume per minute, equivalent to a volume flow across the apical membrane of 1.44 x 10(-6) cm/s, similar in magnitude to the normal rate of fluid absorption by the gallbladder. We determined the mechanism of NaCl entry by varying the ionic composition of the mucosal bath; when most of the mucosal Na+ or Cl- was replaced, cell volume did not increase during pump inhibition. The rate of NaCl entry was a saturable function of Na+ or Cl- in the mucosal bathing solution with K1/2 values of 26.6 mM for Na+ and 19.5 mM for Cl-. The mode of NaCl entry was probably not the parallel operation of Na+-H+ and Cl(-)-HCO-3 exchangers because of the lack of effect of bicarbonate removal or of the inhibitors amiloride and 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonic acid. NaCl entry was reversibly inhibited by bumetanide in the mucosal bathing solution. Transepithelial NaCl and water absorption is the result of the coupled, carrier-mediated movement of NaCl into the cell across the apical membrane and the active extrusion of Na+ by the Na+-K+-ATPase in the basolateral membrane.


1998 ◽  
Vol 275 (4) ◽  
pp. C1067-C1080 ◽  
Author(s):  
Julio A. Hernández ◽  
Ernesto Cristina

The purpose of this study is to contribute to understanding the role of Na+-K+-ATPase and of ionic cotransporters in the regulation of cell volume, by employing a model that describes the rates of change of the intracellular concentrations of Na+, K+, and Cl−, of the cell volume, and of the membrane potential. In most previous models of dynamic cellular phenomena, Na+-K+-ATPase is incorporated via phenomenological formulations; the enzyme is incorporated here via an explicit kinetic scheme. Another feature of the present model is the capability to perform short-term cell volume regulation mediated by cotransporters of KCl and NaCl. The model is employed to perform numerical simulations for a “typical” nonpolarized animal cell. Basically, the results are consistent with the view that the Na+ pump mainly plays a long-term role in the maintenance of the electrochemical gradients of Na+ and K+ and that short-term cell volume regulation is achieved via passive transport, exemplified in this case by the cotransport of KCl and NaCl.


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