par Vanherweghem, Jean-Louis 
;Guerisse, Patrick ;Ducobu, Jean
Référence Renal Physiology, 2, 2, page (65-78)
Publication Publié, 1979
;Guerisse, Patrick ;Ducobu, Jean Référence Renal Physiology, 2, 2, page (65-78)
Publication Publié, 1979
Article révisé par les pairs
| Résumé : | The role of prostaglandins (PG) E2 and F2α on urinary Na excretion was studied in paired isolated dog kidneys which were blood perfused on Nizet's oxygenators. In group I 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 II and in group III experiments, both kidneys were treated with LAS but PGE2 (group II) or PGF2α (group III) was added to the experimental kidneys. In group I, LAS inhibited the spontaneous vasodilatation characterizing the isolated dog kidney perfusion while PGE2 or PGF2α 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 3 groups of experiments. In group I, LAS reduced tubular Na reabsorption rate, presumably at a distal site (clearance studies). PGF2α reduced Na excretion rate in LAS-treated kidneys of group III while PGE2 increased it in similar conditions (group II). In group I, LAS reduced PG levels in the perfusing blood mainly by decreasing PGF2α concentrations. A significant correlation was demonstrated between tubular Na reabsorption rate, expressed as a fraction of Na filtered load, and PGF2α levels. In the isolated dog kidney, Na tubular transport is thus inhibited by PGE2 (hemodynamic or direct tubular effect) while it is enhanced by PGF2α (direct tubular effect). |
