In hypertensive rats, environmental stress causes sodium retention by an ex
aggerated increase in renal sympathetic nerve activity, which is modulated
by angiotensin II. We tested whether similar effects can be observed in hum
ans. In 66 normotensive subjects (half of them with a family history of hyp
ertension) and 36 subjects with mild essential hypertension, urinary sodium
excretion and renal hemodynamics were examined at rest and during mental s
tress treated either with placebo or ACE inhibition in a double-blind, rand
omized, cross-over design. Despite a marked increase in glomerular filtrati
on rate in response to mental stress (Delta glomerular filtration rate, 4.3
+/-7.7 mL/min in normotensives without versus 5.6+/-8.4 mL/min in normotens
ives with a family history versus 10.1+/-5.7 mL/min in patients with mild e
ssential hypertension: P<0.002), the increase in urinary sodium excretion w
as blunted in patients with mild essential hypertension (<Delta>urinary sod
ium excretion, 0.12+/-0.17 mmol/min versus 0.10+/-0.14 mmol/min versus 0.05
+/-0.14 mmol/min; P<0.05), ACE inhibition corrected the natriuretic respons
e to mental stress in subjects with mild essential hypertension (<Delta>uri
nary sodium excretion, 0.05+/-0.14 mmol/min with placebo versus 0.13+/-0.19
mmol/min with ACE inhibition; P<0.01); thus, after ACE inhibition, urinary
sodium excretion increased similarly in all 3 groups. In conclusion. impai
red sodium excretion occurs during mental stress in human essential hyperte
nsion but not in subjects with positive family history of hypertension. Thi
s abnormality in sodium handling during activation of the sympathetic nervo
us system appears to be mediated by angiotensin II.