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K Strange

Publications and source records attributed to K Strange.

60 records · Page 4Linked to original sources
PubMed1987

Absence of significant cellular dilution during ADH-stimulated water reabsorption.

Water reabsorption across many "tight" urinary epithelia is driven by large transepithelial osmotic gradients and is controlled by antidiuretic hormone (ADH). Numerous investigators have concluded that ADH-induced water reabsorption causes large apparent increases in cell volume with concomitant cytoplasmic dilution. A central question in renal physiology has been how cellular homeostasis is maintained in tight urinary epithelia during antidiuresis. Previous direct measurements of cell membrane permeability to water and the present direct measurements of cell volume in collecting tubules of rabbit kidney cortex by quantitative light microscopy show that cell volume does not change significantly during transcellular water flow. Fluid transported across the epithelium accumulated in lateral and basal intercellular spaces; the effect was an increase in cell height and tubule wall thickness accompanied by maintenance of nearly constant cell volume. The stability of cell volume is a consequence of the relatively high water permeability of the blood-facing cell membrane.

Absorption↗
PubMed1987

Cell membrane water permeability of rabbit cortical collecting duct.

The water permeability (Posm) of the cell membranes of isolated perfused rabbit cortical collecting ducts was measured by quantitative light microscopy. Water permeability of the basolateral membrane, corrected for surface area, was 66 microns X sec-1 for principal cells and 62.3 microns X sec-1 for intercalated cells. Apical membrane Posm values corrected for surface area, were 19.2 and 25 microns X sec-1 for principal and intercalated cells, respectively, in the absence of antidiuretic hormone (ADH). Principal and intercalated cells both responded to ADH by increasing Posm of their apical membranes to 92.2 and 86.2 microns X sec-1, respectively. The ratio of the total basolateral cell membrane osmotic water permeability to that of the apical cell membrane was approximately 27:1 in the absence of ADH and approximately 7:1 in the presence of the hormone for both cell types. This asymmetry in water permeability is most likely due to the fact that basolateral membrane surface area is at least 7 to 8 times greater than that of the apical membrane. Both cell types exhibited volume regulatory decrease when exposed to dilute serosal bathing solutions. Upon exposure to a hyperosmotic serosal bath (390 mosM), principal cells did not volume regulate while two physiologically distinct groups of intercalated cells were observed. One group of intercalated cells failed to volume regulate; the second group showed almost complete volume regulatory increase behavior.

Animals↗
PubMed1985

Cellular mechanism of HCO-3 and Cl- transport in insect salt gland.

Active HCO-3 secretion in the anterior rectal salt gland of the mosquito larva, Aedes dorsalis, is mediated by a 1:1 Cl-/HCO-3 exchanger. The cellular mechanisms of HCO-3 and Cl- transport are examined using ion- and voltage-sensitive microelectrodes in conjunction with a microperfused preparation which allowed rapid saline changes. Addition of DIDS or acetazolamide to, or removal of CO2 and HCO-3 from, the serosal bath caused large (20 to 50 mV) hyperpolarizations of apical membrane potential (Va) and had little effect on basolateral potential (Vbl). Changes in luminal Cl- concentration altered Va in a rapid, linear manner with a slope of 42.2 mV/decalog a1Cl-. Intracellular Cl- activity was 23.5 mM and was approximately 10 mM lower than that predicted for a passive distribution across the apical membrane. Changes in serosal Cl- concentration had no effect on Vbl, indicating an electrically silent basolateral Cl- exit step. Intracellular pH in anterior rectal cells was 7.67 and the calculated acHCO-3 was 14.4 mM. These results show that under control conditions HCO-3 enters the anterior rectal cell by an active mechanism against an electrochemical gradient of 77.1 mV and exits the cell at the apical membrane down a favorable electrochemical gradient of 27.6 mV. A tentative cellular model is proposed in which Cl- enters the apical membrane of the anterior rectal cells by passive, electrodiffusive movement through a Cl- -selective channel, and HCO-3 exits the cell by an active or passive electrogenic transport mechanism. The electrically silent nature of basolateral Cl- exit and HCO-3 entry, and the effects of serosal addition of the Cl-/HCO-3 exchange inhibitor, DIDS, on JCO2net and transepithelial potential (Vte) suggest strongly that the basolateral membrane is the site of a direct coupling between Cl- and HCO-3 movements.

Aedes↗
PubMed1984

Mechanisms of CO2 transport in rectal salt gland of aedes. I. Ionic requirements of CO2 secretion.

Rectal salt glands of Aedes dorsalis can be successfully isolated and microperfused in vitro. Microperfused salt glands maintain a large, stable transepithelial potential (-40 to -50 mV, lumen negative) and secrete total CO2 at high and stable rates [CO2 net flux ( JCO2net ) = 799 +/- 57 pmol . min-1 . mm-1]. Bilateral Na+ and K+ or serosal Cl- substitutions and serosal addition of 1.0 mM ouabain, 2.0 mM amiloride, or 0.5 mM 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonic acid had no effect on JCO2net . Removal of luminal Cl- inhibited JCO2net by 80%, whereas serosal addition of 1.0 mM acetazolamide or 0.5 mM 4,4'-diisothiocyano-2,2'-disulfonic acid inhibited JCO2net by 80 and 40%, respectively. Net Cl- reabsorption ( JClnet = -888 +/- 57 pmol . min-1 . mm-1) was equivalent to total CO2 secretion, suggesting that CO2 transport was mediated by a 1:1 exchange of luminal Cl- for serosal HCO-3.

Aedes↗
PubMed1984

Mechanisms of CO2 transport in rectal salt gland of Aedes. II. Site of Cl(-)-HCO3(-) exchange.

In the previous paper [Am. J. Physiol. 246 (Regulatory Integrative Comp. Physiol. 15): R727 - R734 , 1984] evidence was presented that indicated HCO3(-) transport in the microperfused rectal salt gland of Aedes dorslis larvae is mediated by a 1:1 exchange of luminal Cl(-) for serosal HCO3(-). The present work demonstrates clearly that the anterior segment is the site of Cl(-)HCO3(-) exchange. Changes in total CO2 concentration of collected perfusates are the same in perfused anterior segments as in whole, perfused salt glands. Furthermore Cl(-) reabsorption in the perfused anterior segment is equivalent to total CO2 secretion and is completely inhibited by bilateral CO2 and HCO3(-) removal. Contrary to a previous hypothesis, both salt gland segments are capable of secreting strongly hyperosmotic fluids containing high concentrations of Na+, Cl(-), and HCO3(-)-CO3(2-).

Aedes↗