The cellular mechanism and regulation of KC1 reabsorption across the
rectum of the desert locust Schistocerca gregaria has been studied using
tracer fluxes, ion-sensitive microelectrodes, and electrophysiological
techniques. Serosal addition of 1 mM cAMP stimulates transepithelial short-
circuit current (I[sub=SC]) and net Cl absorption (J[sub=net;sup=Cl] ) 10-fold, increases
transepithelial potential (V[sub=t]) 4-fold, and reduces transepithelial resistance
(R[sub=T]) by 40-65%. The properties of locust Cl transport are not consistent with NaCl cotransport models proposed in other epithelia: i) Cl is absorbed from nominally Na-free saline, ii) there is no correlation between trace amounts of
Na contamination and the rate of Cl transport, iii) exposure to cAMP increases
³⁶Cl influx across the apical border into rectal tissue without affecting ²²Na
influx, iv) Cl-dependent I[sub=SC] is not inhibited by 1 mM ouabain (2 h) or 1 mN
furosemide (1 h), v) J[sub=net;sub=Cl] is not affected when the apical Na electrochemical
gradient is reduced by 85%, and vi) there is no relationship between Na and Cl
net electrochemical gradients across the apical membrane. Cl/HCO₃ exchange is
also unlikely since i) Cl-transport is electrogenic, ii) J[sub=net;sub=Cl] is insensitive to CO₂⁻ and HCO₃⁻ removal, and iii) Cl-dependent I[sub=SC] is not inhibited by 1 mM SITS or 1 mM acetazolamide after 1 h exposure. The cAMP-stimulated system is Cl-selective: Cl >> Br >> I,F,SCN,P0₄,SO₄.C₂H₃O₂,urate. The halide sequence suggests a site having high field strength. Cl-dependent I[sub=SC] is inhibited by
low mucosal pH and high osmotic pressure. J[sub=net;sub=Cl] obeys Michaelis-Menten-type
kinetics. Mucosal K increases both the K[sub=m] and V[sub=max] of transepithelial Cl
absorption (K[sub=a] = 5.3 mM K). The active step in J[sub=net;sub=Cl] is at the apical
membrane because net entry of Cl occurs against a large, unfavourable
electrochemical gradient. Serosal cAMP and mucosal K directly stimulate the
active step since both of these agents cause simultaneous increases in J[sub=net;sub=Cl]
and the electrochemical potential opposing CI entry. Passive K transport in the mucosa-to-serosa direction is favoured across apical and basal membranes. Most K absorption (~84%) is electrically coupled to active CI transport under open-circuit conditions, however a small active component is apparent during exposure to cAMP. The response of V[sub=T] to transepithelial salt gradients depends strongly on the direction of the gradients, suggesting that locust rectum is a "tight" epithelium. Intracellular current and fluorescent dye injections reveal strong coupling between rectal cells. Flat-sheet cable analysis indicates that locust rectum becomes "tighter" during cAMP exposure, when transcellular conductance increases from 60 to 95% of the total tissue conductance.
cAMP increases apical membrane K conductance and basal membrane CI conductance. K permeability is inhibited by high (physiological) K and osmotic concentrations. The driving force of CI transport is calculated by two independent methods and the results are interpreted in terms of an equivalent electrical circuit model for KCl reabsorption across locust rectum. / Science, Faculty of / Zoology, Department of / Graduate
| Identifer | oai:union.ndltd.org:UBC/oai:circle.library.ubc.ca:2429/23452 |
| Date | January 1982 |
| Creators | Hanrahan, John William |
| Source Sets | University of British Columbia |
| Language | English |
| Detected Language | English |
| Type | Text, Thesis/Dissertation |
| Rights | For non-commercial purposes only, such as research, private study and education. Additional conditions apply, see Terms of Use https://open.library.ubc.ca/terms_of_use. |
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