Prostaglandins E ₂ and F _2αand Urinary Sodium Excretion in Isolated Dog Kidney

Abstract

The role of prostaglandins (PG) E₂ and F_2α on urinary Na excretion was studied in paired isolated dog kidneys which were blood perfused on Nizet’s oxygenators. In group 1 experiments, lysine acetylsalicylate (LAS), a PG- synthetase inhibitor, was added to the blood perfusing one kidney, the contralateral paired kidney being observed as control. In group 2 and in group 3 experiments, both kidneys were treated with LAS but PGE₂ (group 2) or PGF_2α (group 3) was added to the experimental kidneys. In group 1, LAS inhibited the spontaneous vasodilatation characterizing the isolated dog kidney perfusion while PGE₂ or PGF_2α addition to LAS-treated kidneys restored vasodilatation. No significant difference in glomerular filtration rate between experimental and control kidneys was observed in any of the three groups of experiments. In group 1, LAS reduced tubular Na reabsorption rate, presumably at a distal site (clearance studies). PGF_2α reduced Na excretion rate in LAS-treated kidneys of group 3 while PGE₂ increased it in similar conditions (group 2). In group 1, LAS reduced PG levels in the perfusing blood mainly by decreasing PGF_2α concentrations. A significant correlation was demonstrated between tubular Na reabsorption rate, expressed as a fraction of Na filtered load, and PGF_2α levels. In the isolated dog kidney, Na tubular transport is thus inhibited by PGE₂ (hemodynamic or direct tubular effect) while it is enhanced by PGF_2α (direct tubular effect).