Abstract
The pathophysiological role of renal natriuretic depressor systems and endogenous digitalis like factor (EDLF) on blood pressure (BP) elevation was studied in reduced renal mass rats (RRM) with saline loading for a model of volume dependent hypertension. Fifty-four male Sprague-Dawley rats were operated on to remove varying proportions of their kidney mass (5/6RRM, n=13; 4/6 RRM, n=16; 3/6 RRM, n=12) or sham operated (control, n=13). They were given 1% saline to drink for 4 weeks. BP was elevated significantly at the 1st week in 5/6 RRM and continued to increase until the 4th week, but this was not seen in the other 3 groups. Urine volume (UV) and urinary sodium excretion (UNaV) increased after saline loading in all groups. Urinary kallikrein excretion was significantly lower in order of the 5/6, 4/6 and 3/6 RRM at the basal state and after saline loading. A significant negative correlation was observed between urinary kallikrein and BP. Urinary PGE2 was increased in each RRM in order of the 5/6, 4/6 and 3/6 RRM groups. A significant positive correlation was observed between urinary PGE2 and BP, UV or UNaV. The basal urinary DA excretion was significantly lower in 3 RRMs than in the control. After saline drinking, urinary DA increased in 3 RRMs, while differences disappeared in the control and RRMs. Urinary EDLF increased immediately after the initiation of saline loading in all groups, except the control group, and returned to the basal level 2 weeks later in 3/6 and 4/6 RRM. Only in 516 RRM, the urinary EDLF remained higher than the basal level. A significant positive correlation was found between urinary EDLF and BP or UNaV. From these observations, it was suggested that 1) in 5/6 RRM, EDLF has an important role in the pathogenesis of hypertension, 2) suppressed renal kallikrein-kinin system may have something to do with the BP elevation, and 3) renal PGE2 and DA systems may act to compensate for sodium retention and BP elevation. (Hypertens Res 1995; 18 Suppl. I: S53-S57)
