Abstract
Previous studies have shown that the urinary excretion of prostaglandin (PG) F 2α is stimulated by potassium (K) loading. Because changes of sodium chloride (NaCl) intake also affect renal PG production, in this study we investigated the interaction between the effect of K and that of concomitant reduction of Na and Cl intake. The urinary excretion of PGF 2α and PGE 2 was measured in 12 groups of female rats on normal, high or low K intake. Na and Cl intake were adjusted so that rats had normal intake (controls, C), were selectively Cl depleted (CD), selectively Na depleted (ND) or Na and Cl depleted (NCD). In rats with normal K intake, urinary PGF 2α was not modified by changes of Na or Cl intake, whereas PGE 2 was increased in by Cl depletion (in both NCD ar CD groups). Potassium chloride loading increased urinary PGF 2α and selective Na depletion (ND group) induced a further increase. On the other hand, PGF 2α was not stimulated when K load was associated with Cl depletion. Urine PGF 2α was directly correlated with plasma aldosterone and urinary kallikrein. Urinary PGE 2 did not change with K-loading. The results suggest that PGF 2α participates in the renal adaptation to KCl-loading but not when K is accompanied by non-Cl anions.
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