Renal prostaglandins(PGs) are synthesized in both the cortex and the medulla. PGs modif-·the renal excretion of salts and water. This effects of PGs are related to several different sites of action in the kidney that include : 1) direct inhibitory effects on ion transport in the distaltubule: 2) enhancement of basal water permeability of the collecting tubule and inhibition ofthe hydroosmotic effect of vasopressin. On the other hand, Na-K-ATPase act as carrier of active Na+ transport across the cell membrane.
This study was attempted to investigate the action of PGs on the Na-K-ATPase activity inthe renal cortical homogenate. PG E2 and F2a concentration in the incubation medium were 100,10, 1.0 mg/ml, respectively,
The results obtained are summarized as follows:
1. Total ATPase and Na-K-ATPase activity of the renal cortical homogenate were 15.11 ±0.64 and 1.65 ±0.18㎛/10min/mg protein.
2. Total ATPase activity in PG E2 concentration of 100 rg/´ml was significantly · inhibited as 80.4±5.6% to the control value.
3. PG E2 inhibited the Na-K-ATPase activity. Especially, 1.0㎍/ml in conceniration significantly inhibited the Na-K-ATPase activity as 75.4±19.8 If to the control value.
4. PG F2a also inhibited the Na-K-ATPase activity. Especially. 1,0㎍/ml in concetration significantly different.
From the above results, it was suggested the action of PG E2 and PG F2a on the kidney was mediated by inhibition of renal cortical Ha-K-ATPase activity.
|