Abstract
Abstract
The effect of kallidin (lysyl-bradykinin) on the urinary recovery of sodium-22 was examined in anesthetized, volume-expanded rats. Sodium-22 was microinfused into the lumen of late proximal convoluted tubules with and without kallidin (100 pg/ml). Kallidin enhanced mean sodium-22 recovery from a control of 2.24 ± 0.29% to 6.22 ± 1.30% (δ = 3.98 ± 1.31%, P < 0.005). The urinary recovery of simultaneously microinfused inulin, mean blood pressure, urine flow, and the rate of tubular infusion were similar during control and kallidin microinfusions.
Pretreatment of rats with meclofenamate (3.0 mg/kg) to inhibit renal prostaglandin synthesis blunted, but did not abolish, the effect of kallidin to promote sodium-22 recovery. The changes in sodium recovery induced by kallidin represent a 175 ± 47% and a 58 ± 11% increase from control values in vehicle- and meclofenamate-pretreated rats, respectively. The results indicate that kallidin, microinfused in high doses into the lumen of late proximal tubules, may lower sodium efflux in that nephron. Inhibition of prostaglandin synthesis reduced the tubular effect of kallidin, suggesting that enhanced prostaglandin synthesis may contribute to the natriuretic effects of kallidin. Alternatively, meclofenamate may directly oppose the tubular effect of kallidin.
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