Involvement of the renal kallikrein–kinin system in K +-induced diuresis and natriuresis in anesthetized rats

Abstract

Intravenous infusion of a high-K + solution (67.5 mM KCl, 67.5 mM NaCl) to anesthetized rats increased urine volume by 47.6% after 60 min, compared with infusion of a Na + solution (135 mM NaCl). This treatment also increased urinary excretion of Na + by 32.2%, in parallel with an increase in excretion of K + or Cl −. Urinary excretion of kallikrein increased within 60 min after the start of K + infusion. A bradykinin B 2 receptor antagonist, 8-[3-[ N-[(E)-3-(6-acetamidopyridin-3-yl)acryloylglycyl]- N-methylamino]-2,6-dichlorobenzyloxy]-2-methylquinoline (FR173657; 1.0 mg/kg, i.v.), inhibited the K +-induced diuresis and natriuresis by 41.0% and 26.7%, respectively. These results indicate that K + load induces diuresis and natriuresis through the renal kallikrein–kinin system in rats.