Impaired sodium excretion during mental stress in mild essential hypertension

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.