Cell swelling increases a barium-inhibitable potassium conductance in the basolateral membrane of Necturus small intestine.

Lau, K. R.; Hudson, Randall L.; Schultz, Stanley G.

doi:10.1073/pnas.81.11.3591

Cited by 110 publications

(56 citation statements)

References 19 publications

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“…It is tempting to speculate that basolateral membrane Na+,K+ pump activity and PK may be inhibited pari passu by CAMP. Such coordinated changes in the activity of the two major ion transport pathways in basolateral membranes of epithelial cells have been suggested in other preparations (Lau et al, 1984 ;Hudson and Schultz, 1984).…”

Section: Significance Ofthe Resultsmentioning

confidence: 98%

Cyclic AMP inhibits Cl-/HCO3- exchange at the apical membrane of Necturus gallbladder epithelium.

Reuss

1987

The Journal of General Physiology

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Intracellular microelectrode techniques were employed to study the effect of cyclic AMP on apical membrane Ci-/HCOi exchange and electrodiffusive HCOi transport in Necturus gallbladder epithelium, lntracellular cAMP levels were raised by addition of either the phosphodiesterase inhibitor theophyiline (3 x 10 -s M) or the adenylate cyclase activator forskolin (10 -5 M) to the serosal bathing solution. Measurements of pH in a poorly buffered control mucosal solution upon stopping superfusion show acidification, owing to secretion of both H + and HCOL When the same experiment is performed after addition of amiloride or removal of Na + from the mucosal bathing medium, alkalinization is observed since H + transport is either inhibited or reversed, whereas HCOi secretion persists. The changes in pH in both amiloride or Na-free medium were significantly decreased in theophylline-treated tissues. Theophylline had no effect on the initial rates of fall of intracellular CIactivity (aCl 0 upon reducing mucosal solution [CI-] to either 10 or 0 mM, although membrane voltage and resistance measurements were consistent with stimulation of apical membrane electrodiffusive CI-permeability. Estimates of the conductive flux, obtained by either reducing simultaneously mucosal [CI-] and [HCOg] or lowering [C1-] alone in the presence of a blocker of anion exchange (diphenylamine-2-carboxylate), indicate that elevation of intracellular cAMP inhibited the anion exchanger by ~50%. Measurements of net CI-uptake upon increasing mucosal C1-from nominally zero to levels ranging from 2.5 to 100 mM suggest that the mechanism of inhibition is a decrease in Vmax. Consistent with these results, the rate of intracellular alkalinization upon reducing external C1-was also inhibited significantly by theophylline. Reducing mucosal solution [HCO~] from 10 to 1 mM under control conditions caused intracellular acidification and an increase in aCll. Theophylline inhibited both changes, by 62 and 32%, respectively. These data indicate that elevation of intracellular cAMP inhibits apical membrane anion (CI-/HCOg) exchange. Studies of the effects of rapid changes in mucosal [HCOg] on membrane voltages and the apparent ratio of membrane resistances, both in the presence and in Address reprint requests to Dr.

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Section: Significance Ofthe Resultsmentioning

confidence: 98%

Cyclic AMP inhibits Cl-/HCO3- exchange at the apical membrane of Necturus gallbladder epithelium.

Reuss

1987

The Journal of General Physiology

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“…However, since the stretch-sensitive ion channels are influenced by shear and tensile stresses in the cell membrane (25)(26)(27), the effect of osmolarity at higher tensile membrane stress should be studied. Interference microscopy may also help in the study of the effects of stretch on growth (28)(29)(30)(31) and biochemical processes and gene expression (32)(33)(34).…”

Section: Discussionmentioning

confidence: 99%

On measuring the third dimension of cultured endothelial cells in shear flow.

Liu¹,

Yen²,

Fung³

1994

Proc. Natl. Acad. Sci. U.S.A.

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The stress in the endothelial cells induced by blood flow depends on the waviness of the blood-endothelium interface and the slopes at the junctions of neighboring cells in the direction of flow. The height and slope in the third dimension of the living endothelial cells cannot be measured by ordinary optical and electron microscopy. Here we show that interference microscopy meets the challenge. We measured the geometry of cultured confluent human vascular endothelial cells in a flow, and we found that in a normal section parallel to the flow, the absolute values of the surface slopes at the cell junctions were 0.70 ± 0.02 (SE) and 0.80 ± 0.02 (SE) at the leading and trailing edges of the cells, respectively, in a culture medium of osmolarity 310 mosM with a shear stress of approximately 1 N/M2. A reversal of the flow direction led to a reversal ofthe slope pattern. An increase in medium osmolarity above 310 mosM induced an initial decrease in the slopes followed by a return to normal, whereas a decrease in the osmolarity had a reversed effect. These results, in light of our previous theoretical analyses, show that tensile stress exists in the endothelial cell membrane, and that the mechanism of tension accumulation is a reality. The accumulation is not 100% because the membranes are not smooth at the cell junctions.the membrane of cell i + 2 must bear not only the shear acting on it directly but also the cumulative tension in the membrane of cell i + 1. In either case the mechanism of accumulation can become serious because hundreds of thousands of cells are on line. The reality is closer to Fig. 1A. Ifthe in vivo blood shear is 1 N/M2, then the tension in the cell membrane can be 104 N/M2 or larger, which causes a shear stress of 5 x 103 N/M2 or larger acting on planes inclined at 450 to the direction of tension. If integrins or ion channels were lined up with these inclined planes, they could, theoretically, be sensitive to the large shear stress. Thus the significance is seen.In the past, the significance of the membrane geometry of the endothelial cells was unknown, and there is no known method for its determination. An atomic force microscope may be applied (8), but it is difficult to use it in a flowing fluid. Electron microscopy requires tissue fixation and dehydration, which can induce geometric distortion. Facing these difficulties, we recalled our early work on the determination of the thickness profile of erythrocytes by using a MachZender interference microscope (9-13), which yielded data with a resolution of 0.02 ,um based on physical optics. Hence we hypothesized that it might yield the endothelium profile. This paper is concerned with the geometric shape of the interface between flowing blood and a blood vessel. The endothelium, which is a confluent layer of endothelial cells, is the biological gateway between the blood and the tissues and organs of the body and is the source of many factors that are critical to health and disease such as atherosclerosis. As sketched in Fig. 1, each endot...

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“…Models for cellular signalling in RVD were proposed by and MacLeod (1994), assigning a function to increased cytosolic free calcium, metabolism of arachidonic acid, synthesis of prostaglandin E2 (PGEµ) and leukotriene D4 (LTDÚ), activation of protein kinases and the Ca¥-calmodulin complex. The recent literature has provided much evidence to support these models, in particular concerning intestinal cells in Necturus small intestine (Lau et al 1984), enterocytes from guinea-pig jejunum (MacLeod & Hamilton, 1991), rat colonic crypts (Diener et al 1992), small intestinal guineapig crypts (O'Brien et al 1991) or cultured human epithelial cells (Intestine 407) (Hazama & Okada, 1988), but most of these studies remain fragmentary, generally focusing on membrane conductances only.…”

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confidence: 99%

Volume regulation following hypotonic shock in isolated crypts of mouse distal colon

Mignen

Gall

Harvey

et al. 1999

The Journal of Physiology

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The crypts of distal colon are submitted to frequent cell volume modifications resulting from fluctuating entry or exit of ion solutes and osmotically obliged water, and from variations in the osmotic pressure in the luminal compartment of the colon. The osmotically induced variations in crypt cell volume are rapidly compensated by uptake or efflux of osmotically active molecules. Thus, exposure of colon crypts to hypotonic media causes cell swelling followed by regulatory volume decrease (RVD) (Diener & Scharrer, 1995 1. A video-imaging technique of morphometry was used to measure the diameter as an index of cell volume in intact mouse distal colon crypts submitted to hypotonic shock. 2. Transition from isotonic (310 mosmol l¢) to hypotonic (240 mosmol l¢) saline caused a pronounced increase in crypt diameter immediately followed by regulatory volume decrease (RVD). 3. Exposure of crypts to Cl¦-free hyposmotic medium increased the rapidity of both cell swelling and RVD. Exposure of crypts to Na¤-free hyposmotic medium reduced the total duration of swelling. Return to initial diameter was followed by further shrinkage of the crypt cells. 4. The chloride channel inhibitor NPPB (50 ìÒ) delayed the swelling phase and prevented the subsequent normal decrease in diameter. 5. The K¤ channel blockers barium (10 mÒ), charybdotoxin (10 nÒ) and TEA (5 mÒ) inhibited RVD by 51, 44 and 32%, respectively. 6. Intracellular [Ca¥] rose from a baseline of 174 ± 17 nÒ (n = 8) to 448 ± 45 nÒ (n = 8) during the initial swelling phase 7. The Ca¥ channel blockers verapamil (50 ìÒ) and nifedipine (10 ìÒ), the chelator of intracellular Ca¥ BAPTA AM (30 ìÒ), or the inhibitor of Ca¥ release TMB-8 (10 ìÒ), dramatically reduced volume recovery, leading to 51% (n = 9), 25% (n = 7), 37% (n = 6), 32% (n = 8) inhibition of RVD, respectively. TFP (50 ìÒ), an antagonist of the Ca¥-calmodulin complex, significantly slowed RVD. The Ca¥ ionophore A23187 (2 ìÒ) provoked a dramatic reduction of the duration and amplitude of cell swelling followed by extensive shrinkage. The release of Ca¥ from intracellular stores using bradykinin (1 ìÒ) or blockade of reabsorption with thapsigargin (1 ìÒ) decreased the duration of RVD. 8. Prostaglandin E2 (PGE2, 5 ìÒ) slightly delayed RVD, whereas leukotriene DÚ (LTD4, 100 nÒ) and arachidonic acid (10 ìÒ) reduced the duration of RVD. Blockade of phospholipase A2 by quinacrine (10 ìÒ) inhibited RVD by 53%.

show abstract

Cell swelling increases a barium-inhibitable potassium conductance in the basolateral membrane of Necturus small intestine.

Cited by 110 publications

References 19 publications

Cyclic AMP inhibits Cl-/HCO3- exchange at the apical membrane of Necturus gallbladder epithelium.

Cyclic AMP inhibits Cl-/HCO3- exchange at the apical membrane of Necturus gallbladder epithelium.

On measuring the third dimension of cultured endothelial cells in shear flow.

Volume regulation following hypotonic shock in isolated crypts of mouse distal colon

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