Aldosterone in the exaggerated natriuresis of spontaneously hypertensive rats.

The effect of mineralocorticoid hormones on the urinary responses of spontaneously hypertensive and normotensive rats to oral salt loading was determined. In response to a control salt load, the increase was determined. In response to a control salt load, the increase in urinary sodium excretion by the spontaneously hypertensive rats was significantly greater than that of the normotensive rats [48 +/- 6 (SE) mueq/h vs. 26 +/- 4 mueq/h]. Treatment with spironolactone did not significantly alter the natriuretic response of the spontaneously hypertensive rats (43 +/- 8 mueq/h) to another salt load, but increased the natriuretic response of the normotensive rats (55 +/- 7 mueq/h) to that of the hypertensive rats. D-Aldosterone suppressed the natriuretic response to salt loading of the hypertensive rats to a level which was not significantly different from that of the normotensive rats. Plasma aldosterone concentration was significantly lower in the spontaneously hypertensive rats than in the normotensive rats (18.0 +/- 3.3 and 52.1 +/- 5.2 ng/100 ml, respectively). Neither extracellular fluid volume nor total body water in spontaneously hypertensive and normotensive rats were significantly different. The data support the hypothesis that the exaggerated natriuresis in the spontaneously hypertensive rats is mediated by a relative lack by these rats of aldosterone-mediated distal tubular sodium reabsorption.