Renin-angiotensin-aldosterone system in exaggerated natriuresis of chronic glomerulonephritis.

Abstract

Angiotensin II (AII) and aldosterone (Aldo) in plasma, blood pressure (BP) and urinary excretion of sodium were studied before, during and in two periods after intravenous sodium loading with 500 ml of sodium chloride solution (50 g/l) in 11 normotensive and 10 hypertensive patients with histologically verified chronic glomerulonephritis and creatinine clearance in the range from 11 to 167 ml/min, and in 10 normotensive control subjects. The absolute increase of sodium excretion during loading was higher in the patients grouped together and in the hypertensives alone, but not in the normotensive patients when compared with the control subjects. No correlation was found between sodium excretion and control mean BP or change in mean BP during loading. AII and Aldo were suppressed during loading in both patients and control subjects. In the patients but not in the control subjects the increase of sodium excretion correlated positively with pre-infusion value of AII and negatively with change in AII during the sodium loading. No correlation was found between sodium excretion and Aldo and changes of Aldo. In conclusion, the results might suggest that the renin-angiotensin system is involved in the regulation of exaggerated natriuresis in chronic glomerulonephritis.