Effect of sodium and chloride depletion on urinary prostaglandin F2α excretion in potassium loaded rats

Previous studies have shown that the urinary excretion of prostaglandin (PG) F2 alpha 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 PGF2 alpha and PGE2 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 PGF2 alpha was not modified by changes of Na or Cl intake, whereas PGE2 was increased in by Cl depletion (in both NCD or CD groups). Potassium chloride loading increased urinary PGF2 alpha and selective Na depletion (ND group) induced a further increase. On the other hand, PGF2 alpha was not stimulated when K load was associated with Cl depletion. Urine PGF2 alpha was directly correlated with plasma aldosterone and urinary kallikrein. Urinary PGE2 did not change with K-loading. The results suggest that PGF2 alpha participates in the renal adaptation to KCl-loading but not when K is accompanied by non-Cl anions.     

Polymorphism due to variable number of repeats in the human involucrin gene.

The coding region of the involucrin gene in higher primates contains a segment consisting of numerous tandem repeats of a 10-codon sequence. The process of repeat addition began in a common ancestor of all higher primates and subsequent repeats were added vectorially. As a result, the principal site of repeat addition has moved in the 3' to 5' direction and the most recently generated repeats (the late region) are close to the 5' end of the segment of repeats. In the human, most of the late region is made up of two different blocks, each consisting of nearly identical repeats. We describe here five polymorphic forms resulting from the addition of differing numbers of repeats to each block. As the variety and nature of the polymorphic alleles are different in different human populations, we postulate that the process of repeat addition is genetically determined.