M. Shalmi et al., MODEL EXPLAINING THE RELATION BETWEEN DISTAL NEPHRON LI+ REABSORPTIONAND URINARY NA+ EXCRETION IN RATS, American journal of physiology. Renal, fluid and electrolyte physiology, 43(3), 1998, pp. 445-452
Li+ may be reabsorbed via an amiloride-sensitive mechanism in the coll
ecting ducts of rats administered a low-Na+ diet. This was investigate
d by measuring the increase in fractional urinary excretion of Li+ (FE
Li) in response to amiloride in conscious rats at two different levels
of plasma Li+ concentration and after administration of bendroflumeth
iazide (BFTZ), angiotensin III (ANG III), and aldosterone (Aldo). The
results confirmed that amiloride increased (FELi) in rats on a low-Na diet (20 +/- 1 to 35 +/- 1%, means +/- SE), whereas no increase was o
bserved in rats on a normal Na+ diet (37 +/- 1 to 38 +/- 1%). The lith
iuretic effect of amiloride was 1) abolished by preadministration of B
FTZ (32 +/- 1 to 33 +/- 2%) to Na+-deprived rats and 2) increased by A
NG III (27 +/- 3 to 33 +/- 2%) and Aldo (25 +/- 2 to 37 +/- 2%) in Na-replete rats. Amiloride-induced changes in FELi were independent of p
lasma Li+ concentration but inversely related to the fractional excret
ion of Na+ and the amiloride-sensitive excretion of K+. These results
are compatible with the hypothesis that a low tubular Na+ concentratio
n reduces end-tubular Na+ reabsorption and results in hyperpolarizatio
n of the apical membrane, thus favoring Li+ uptake into the cells.