We investigated renal and peripheral forearm extraction of atrial natr
iuretic peptide in patients with primary aldosteronism to determine wh
ether alterations in extraction may contribute to the elevated levels
of circulating atrial natriuretic peptide observed in primary aldoster
onism. We obtained simultaneous venous blood samples from the left ren
al vein and a peripheral vein and from the radial artery in 28 patient
s with primary aldosteronism and 10 patients with essential hypertensi
on. Renal extraction of atrial natriuretic peptide was significantly (
P<.001) reduced (40+/-2%) in primary aldosteronism compared with essen
tial hypertensive patients (62+/-3%). Peripheral forearm extraction wa
s also reduced (P<.01) in primary aldosteronism compared with essentia
l hypertensive patients (24+/-3% versus 38+/-4%). These findings are c
onsistent with widespread downregulation of atrial natriuretic peptide
receptors in primary aldosteronism. Consistent with reports that mark
ed reduction in glomerular filtration rate is required before the rena
l extraction of atrial natriuretic peptide is reduced, no significant
relationship between renal extraction of atrial natriuretic peptide an
d plasma creatinine was seen in primary aldosteronism or essential hyp
ertension. Although the major regulators of atrial natriuretic peptide
secretion in primary aldosteronism are presumably alterations in arte
rial blood pressure and plasma volume, reduced renal and peripheral ex
traction of atrial natriuretic peptide in primary aldosteronism may al
so contribute significantly to the elevated circulating levels observe
d.