Enhanced Blood Pressure Response to Mineralocorticoid Stimulation in Normotensive Members of Hypertensive Families

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Abstract
Currently normotensive offspring of essential hypertensive parents often have disturbances in blood pressure (BP) regulation such as abnormalities in electrolyte homoeostasis, increased salt-sensitivity and/or impaired renal Na+-excretion. Whether an altered reactivity to mineralocorticoids may also play a role is presently unknown. Therefore, we investigated BP (recorded during 24 h), plasma atrial natriuretic factor (ANF), cyclic guanosine monophosphate (cGMP), aldosterone (PA) and renin activity (PRA), 24-h urine electrolyte and cGMP excretions measured on 4 consecutive days, as well as other variables, after I week on placebo and after 3 weeks of 9α-fludrocortisoneacetate (9αF) administration, 0.6 mg/d in 12 normotensive sons of essential hypertensive parents (SEH) and 12 body-mass-index- and age-matched (25 ±1[± SEM]yr) sons of normotensive parents (SN). On placebo, the 2 groups did not differ significantly in average 24 h BP (mean BP 95 ± 2 vs 95 ± 2 mmHg), plasma-ANF (40 ± 7 vs 30 ± 5 pg/ml), cGMP (6 ± 0.4 vs 6 ±0.5 nmol/1), PRA (1.3 ± 0.1 vs 1.6 ± 0.2 ng/ml/h), PA (9 ± 0.5 vs 10 ± 0.9 ng/dl), hematocrit (44 ±0.7 vs 44 ± 0.4%) and 96-h urinary-Na+ (mean 205 ± 19 vs 195 ± 16mmol/d), -K+ (69 ± 6 vs 78 ± 7 mmol/d) or -cGMP (461 ± 35 vs 483 ± 32 nmol/d). 9αF significantly increased BP in SEH (p < 0.005) but not SN (107 ± 2 vs 100 ± 2 mmHg, pp+ (205 ± 19 vs 195 ± 17 mmol/d)-K+ (80 ± 8 vs 69 ± 6 mmol/d) or -cGMP (673 ± 76 vs 653 ± 62 nmol/d), plasma-Na± (increase + 3 vs + 2 mmol/1), K+ (decrease –0.5 vs –0.5 mmol/1), hematocrit (42 ± 0.8 vs 42 ±0.2%) or body weight (increase + 2.0 vs + 1.9 kg). These results indicate that normotensive offspring of hypertensive parents may react to mineralocorticoid stimulation with an enhanced BP-increase. This disturbance cannot be explained by insufficient renin-aldosterone suppression, inadequate ANF stimulation or abnormally increased N+ -fluid retention.