Plasma volume (PV) and extracellular fluid volume (ECF) were determined in 7 patients with
essential hypertension (controls) and in 10 patients with primary
aldosteronism, while on a high Na diet (342 mEq/day) and on a low Na diet (12 mEq/day). The volume studies were repeated in 6 of the primary
aldosteronism patients during treatment with
spironolactone for over 3 months. Plasma
renin activity (PRA), plasma
aldosterone concentration (PAC),
cortisol concentration, and serum Na and K concentrations were measured in all patients while on a Na-restricted diet (85 mEq/day) as well as on high-Na and low-Na diets. There were no significant changes in arterial pressure during different Na diets in any groups of patients with
essential hypertension, or primary
aldosteronism with and without
spironolactone therapy.
Spironolactone treatment normalized the arterial pressure in patients with primary
aldosteronism at all Na intakes. These patients had greater values for PV and ECF than did those with
essential hypertension.
Spironolactone treatment reduced PV during the low-Na diet, but did not alter it during the high-Na diet.
Spironolactone did not produce significant changes in ECF during either the high-Na or low-Na diets. Although there were no changes in PV and ECF in patients with primary
aldosteronism due to changes in Na intake, both PV and ECF were significantly less in these patients during
spironolactone treatment and in patients with
essential hypertension during low-Na intake than during high-Na intake. With primary
aldosteronism, PRA was depressed and PAC was elevated when compared to
essential hypertension, these were not altered by different Na diets in the patients with primary
aldosteronism as they were in those with
essential hypertension. During treatment with
spironolactone the PRA was restored to normal and showed normal changes with variations in dietary Na, but PAC remained elevated during
spironolactone. Plasma
cortisol was the same among those with
essential hypertension and patients with untreated and
spironolactone-treated primary
aldosteronism. Serum K was less in untreated primary
aldosteronism during all Na diets than in
essential hypertension, but during
spironolactone it was restored to normal. These results suggest that in primary
aldosteronism the reduction in arterial pressure by
spironolactone treatment does not occur simply by reductions in body fluid volumes. The long-term treatment of patients with primary
aldosteronism with
spironolactone does not inhibit the production of
aldosterone, possibly because of enhanced activity of the renin-angiotensin system and an increase in serum K.