Amiloride and sodium fluxes across fish gills in fresh water and in sea water.
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Biomedical subjects
Publications and source records attributed to J Maetz.
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1. Removal of calcium from Carassius either with chelating agents or by adaptation to deionized water increased sodium influx through the gills twofold.2. Treatment of fish with chelating agents increased sodium outflux, whereas adaptation to deionized water reduced sodium outflux. The effects on outflux do not appear to result from calcium removal.3. Addition of calcium (2-20 mM) reversed the effects on influx of chelating agents and of adaptation to deionized water.4. Magnesium (2-10 mM) was without significant effect on sodium influx, but increased the outflow in fish adapted to deionized water.
1. The sodium influx through the gills of eels placed in calcium-free sea water for 15 hr was double that of controls. The effect was reversed in 1 hr by addition of calcium.2. The total sodium outflux through the gills of fish placed in calcium-free sea water for 15 hr was double that of controls. The effect was only partially reversed in 15 hr by addition of calcium.3. The passive outflux component of the total outflux was increased fourfold when calcium was removed and was restored to normal in 15 hr by addition of calcium. The active (exchange) outflux component of the total outflux was halved by calcium removal and increased above normal following calcium addition.4. The inability of calcium to restore the total outflux to normal within 15 hr in calcium-depleted fish, together with the raised plasma sodium concentration at this time, suggests that the raised outflux is caused by homoeostatic mechanisms, rather than permeability changes in the gill epithelium.
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The net sodium extrusion rate by the gill of the seawater-adapted euryhaline flounder is identical to the potassium influx. The excretion of sodium is blocked in K(+)-free seawater solutions. The instantaneous sodium outflux readjustment pattern of flounders transferred from seawater to solutions of various sodium chloride or potassium chloride concentrations is consistent with the hypothesis of a linkage between Na(+) outflux and K(+) influx through a common exchange carrier. External Na(+) and K(+) compete for this comnmonz carrier. It is suggested that the exchange diffusion mechanism (linkage of sodium influx and outflux) and the high internal sodium turnover rate which characterizes all seawater teleosts are the results of this competitive process. The sodium-potassium dependent adenosine triphosphatase system occurring in the gill of the seawater teleosts may play a central role in this sodium-potassium exchange pump.
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The sea water (SW)-adapted euryhaline Platichthys flesus, and the marine Serranus exchange about 50% of their internal sodium with the external sodium per hour. This rate of exchange decreases with decreasing salinity of the adaptation medium. When the flounder is transferred from SW to FW an instantaneous 90% reduction of the Na and Cl outflux is observed. About 30 min later a second, progressive, reduction occurs. The outflux reductions appear to result from two types of regulatory mechanisms reducing gill permeability and preventing excessive salt loss. The first reduction corresponds to independent "Na- and Cl-free effects" as shown by transfers to artificial media containing either Na or Cl with an impermeant co-ion. The pattern of simultaneous rapid variations of Na influx and outflux for a range of salinity changes in flounder adapted to SW, 1/2 SW, or 1/4 SW has been studied. The data are compatible with the hypothesis of an exchange diffusion mechanism characterized by a coupling of both unidirectional fluxes. The affinity of the exchange diffusion carrier for sodium has been measured (Km approximately equal to 400 mM). The delayed reduction would result from a progressive diminution of the quantity of carrier available but without modification of its affinity for sodium. When the stenohaline marine perch is transferred from SW to FW, a 40% reduction of the outflux is observed. But it is not the result of an exchange diffusion effect as it is related to the external osmolarity change and not to the NaCl concentration change. Furthermore no delayed reduction is observed after transfer into FW. This transfer is accompanied by a heavy loss of electrolytes resulting in a rapid decline of the plasma electrolyte level and death. A comparative survey of the relative importance of these regulatory mechanisms has been made.