Evidence that alterations in distal sodium delivery and distal sodium avidity affect the rate of excretion of an acute HCl load.
In these experiments, two groups of animals were studies to evaluate the effect of altering renal tubular sodium-handling on the excretion of acute HCl load. In group, I, normal salt animals hypotonically expanded with antidiuretic hormone (ADH) (using a protocol known to stimulate aldosterone) presented large amounts of sodium to the distal tubule and excreted an acute HCl load much more efficiently than did animals pretreated with either a normal (NL) or low (LO) salt diet alone. In group II, 24 hr after acid-loading, the plasma bicarbonate concentrations were significantly lower in animals pretreated with sodium restriction plus furosemide (F) than in those maintained on a normal (NL) or high (HI) salt diet alone. Acid excretion was maximized (ADH) when distal sodium avidity was stimulated in the presence of adequate distal sodium delivery and minimized (F) when distal sodium delivery was limited (despite possible augmentation of distal sodium avidity). Alterations in urinary sodium excretion alone (LO, NL, HI) did not affect the rate of acid excretion. These data are compatible with the hypothesis that the excretion of an acute HCl load is mediated by existing levels of distal sodium delivery and distal sodium avidity.
D000042:Absorption; D000818:Animals; D001639:Bicarbonates / Q000097:blood; D002712:Chlorides / Q000097:blood; D004285:Dogs; D005260:Female; D006851:Hydrochloric Acid / Q000378:metabolism*; D007684:Kidney Tubules / Q000378:metabolism*; D007686:Kidney Tubules, Distal / Q000378:metabolism*; D011188:Potassium / Q000097:blood; D012964:Sodium / Q000097:blood / Q000378:metabolism*
D001639:Bicarbonates; D002712:Chlorides; D012964:Sodium; D006851:Hydrochloric Acid; D011188:Potassium