Role of dietary potassium in the hyperaldosteronism and hypertension of the remnant kidney model

The remnant kidney model of progressive renal disease is marked by arterial hypertension, especially when produced by nephrectomy and partial infarcti on. Hyperaldosteronism sustains much of the hypertension, but the stimuli t o the increased aldosterone levels are uncertain. It is hypothesized that t he hyperaldosteronism attending this model stems from the combination of fi xed dietary potassium load in the face of reduced filtration on the one han d, and persistent renin secretion from the scarred remnant kidney on the ot her. This hypothesis predicted that dietary potassium restriction would low er aldosterone and BP in this model. To test this prediction, two groups of rats with a remnant kidney were studied. Group 1 consumed 0.4 +/- 0.06 mEq (mean +/- SD) of potassium chloride daily, and group 2 ate 4.8 +/- 1.0 mEq daily. Two sham-operated groups with intact kidneys also were studied. Gro up 3 consumed 1.7 +/- 0.2 mEq daily and group 4 ate 15.2 +/- 1.4 mEq daily. These levels of intake were designed to provide at least as much potassium per liter of GFR in the sham groups as in the remnant kidney rats. Systoli c BP (SBP), 24-h protein excretion, plasma aldosterone levels, 24-h urinary aldosterone excretion, and plasma renin activity (PRA) were determined in all groups at 2 wk. At 4 wk, after SEP and protein excretion measurements, remnant kidneys were perfusion-fixed for morphometric analysis. SEP was nor mal in both sham-operated groups and was not different between the groups ( 113 +/- 13 versus 117 +/- 2 mmHg, group 3 versus group 4). In the remnant a nimals, SEP at 2 wk followed potassium intake: Group I had a lower SEP than group 2 (140 +/- 26 versus 170 +/- 34 mmHg, P = 0.005). The same SEP patte rn persisted at 4 wk(153 +/- 25 versus 197 +/- 27 mmHg, group 1 versus grou p 2, P = 0.0006). However, 24-h urinary protein excretion was not different between the two groups with remnant kidneys at either 2 or 4 wk. Both plas ma and 24-h urinary aldosterone excretion at 2 wk followed potassium intake (120 +/- 124 versus 580 +/- 442 pg/ml for plasma aldosterone, group 1 vers us group 2, P = 0.03, and 2.6 +/- 1.8 versus 23.2 +/- 9.8 ng/d for urinary aldosterone, group I versus group 2, P = 0.0001). PRA, however, followed a reverse pattern in which dietary potassium restriction resulted in higher l evels (16 +/- 6 versus 6 +/- 3 ng angiotensin I/ml per h, group 1 versus gr oup 2, P = 0.01). A similar pattern for PRA and aldosterone excretion was a lso observed in the sham groups, in which lower potassium intake also resul ted in a significantly higher PRA and lower aldosterone excretion. The cons tancy of BP in the sham groups likely reflects their lack of nephron reduct ion and greater sodium excretory capacity. Morphometric analysis in remnant animals revealed no significant difference between the two dietary groups in the prevalence of glomerular sclerosis, glomerular volume, or interstiti al volume. It is concluded that dietary potassium is a potent determinant o f hypertension in the remnant kidney model probably through the actions of aldosterone and that the high aldosterone secretion in this model is a func tion of the dietary potassium load. In this model, reduction in nephron num ber is also critical in promoting hypertension in conjunction with hyperald osteronism.