段階的腎摘高血圧ラットの昇圧機転に関わる内因性digitalis様因子及び腎prostaglandin系の役割
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We have previously reported that 5/6 reduced renal mass rats (RRM), a model of volume dependent hypertension, show blood pressure elevation and continuous increase of urinary endogenous digitalis like factor (EDLF) excretion compared to 4/6, 3/6 RRM and sham operated rats (Sham). On the other hand, urinary prostaglandin (PG) E? was observed to rise at about the same rate in 5/6 and 4/6 RRM. The roles of EDLF and renal PGE? were investigated in order to clarify the pathogenesis of the high blood pressure observed in 5/6 RRM. The effect of chronic intraperitoneal infusion of ouabain (0.05 mg/kg/day) for 14 days on systolic blood pressure (SBP) and urinary sodium excretion (UNaV) was investigated in 4/6 RRM and Sham. No change in SBP was observed in either 4/6 RRM with vehicle, or Sham with vehicle. In the ouabain treated groups, significant SBP elevation (126±4 to 158±8 mmHg ; p<0.05) was obser- ved in 4/6 RRM, but not in Sham. Four sixths RRM treated with ouabain maintained an augmented urinary sodium excretion, which was significantly higher than in 4/6 RRM with vehicle (p<0.05). There was a significant positive correlation between SBP and UNaV (p<0.01). Therefore, it appears that in 4/6 RRM, which show impaired renal sodium handling though their blood pressure remains within the normal range, the observed blood pressure elevation and augmentation of urinary sodium excretion may be due to the suppression of the Na-K-ATPase activity by ouabain. The effect of chronic intraperitoneal administration of indomethacin (6 mg/kg/day) for 14 days on SBP, urinary PGE? excretion and UNaV was also evaluated in 4/6 RRM and Sham. In the in- domethacin treated groups, significant SBP elevation (119±4 to 144±5 mmHg ; p<0.05) was obser- ved in 4/6 RRM, but not in Sham. No change in SBP was observed in either 4/6 RRM with vehicle, or Sham with vehicle. There was a significant negative correlation between the change in SBP and that in urinary PGE? excretion (p=0.01) in 4/6 RRM. This suggests that the augmented urinary PGE? excretion which was observed in 4/6 RRM may play a compensatory role for the blood pressure elevation. On the other hand, the change of UNaV in 4/6 RRM treated with indomethacin (-15.7±2.7mEq/kg/ day) was significantly larger than in the 4/6 RRM treated with vehicle (-8.5±1.2mEq/kg/day) (p<0.05). There was a significant positive correlation between the change of urinary PGE? excre- tion and that of UNaV (p<0.01). Moreover, there was a significant negative correlation between the change of UNaV and that of SBP (p<0.01). These results indicate that the inhibition of PGE? production in 4/6 RRM may decrease renal sodium excretion and cause elevated blood pressure. From these data, we infer that the augmented urinary PGE? excretion which was observed in 4/6 RRM plays a compensatory role for impaired renal sodium handling and also blood pressure eleva- tion. In conclusion, increased EDLF might be an important factor in the etiology of hypertension in 5/6 RRM, and PGE? may play a compensatory role against elevated blood pressure.
- 1992-08-01
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