Abstract
Amiloride (3,5-diamino-6-chloropyrazinoyl-guanidine) was found to inhibit the unidirectional flux of 22Na in perfused proximal tubules of rats when the drug was present in the blood (1). The drug did not inhibit the net water reabsorption, therefore, it apparently did not have an affect on the active reabsorption of sodium.
Since amiloride has been found to be a potent inhibitor of sodium reabsorption in the amphibian bladder and skin (2, 3) and since it has been found by the same authors that the inhibition of sodium transport is about one thousand times higher when the drug is on the source than when it is on the sink site of the sodium transport, experiments were designed to test the effect of the drug when present in the luminal and not in the interstitial site of the tubule cell.
Methods. Sprague-Dawley rats weighing about 200 g were anesthetized with Inactin (100 mg/kg body wt.) and then infused through the right jugular vein with Ringer's solution at a rate of 30 ml/hr-kg. Using a modification of the microperfusion technique and apparatus of Sonnenberg and Deetjen (4), proximal tubules were perfused at a rate of 20 nanoliters per min.
Two pumps were used, one contained a control solution (Ringer's with 22Na and 14Cinulin) and the other contained the same solution plus 10-4 amiloride. A selected proximal tubule was first perfused with the control solution for 30-40 rnin, and 2-4 samples were obtained during this period. Then the control pump was withdrawn and substituted by the “amiloride” pump. Perfusion was restarted at exactly the same location. The amiloride perfusion was administered for 45-60 min during which time 2-4 samples were obtained. The use of the 2 pumps was randomized with reference to their use for control or for amiloride perfusions.
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