ABNORMALITIES IN THE RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM IN NORMOTENSIVE SUBJECTS WITH A POSITIVE FAMILY HISTORY OF HYPERTENSION

Non-hypertensive men with a positive family history of hypertension in two generations (N = 16) were compared with weight-matched (N = 13) a nd lean (N = 12) control groups with a negative family history of hype rtension with respect to the activity of the renin-angiotensin-aldoste rone system at baseline and during an oral glucose tolerance test. Blo od pressure was measured phonographically after 30 min of semirecumben t rest and the oral glucose tolerance test was performed after a 10-h overnight fast with 100 g of glucose given orally. Blood samples were drawn from a peripheral catheter at baseline, 30 and 120 min after the glucose challenge. Systolic and diastolic blood pressures did not dif fer between subjects with a positive or a negative family history of h ypertension. At baseline, blood glucose and plasma insulin were simila r in the three groups while the group with a positive family history o f hypertension had a significantly lower plasma renin activity (PRA) ( 0.85 +/- 0.09 compared with the weight-matched but not with the lean c ontrol group (1.36 +/- 0.13 and 1.06 +/- 0.15 ng AI.ml(-1).h(-1); p < 0.01 and NS, respectively). The PRA increased significantly after the glucose challenge in all groups (p < 0.01), while the plasma aldostero ne concentration decreased after 30 min and then showed an increase at 120 min. The PRA response was less pronounced in the group with a pos itive family history of hypertension compared with the weight-matched and lean control groups (p < 0.05 and p < 0.01, respectively). Serum p otassium did not change significantly in either group after the glucos e challenge. Urinary sodium excretion was similar in the three groups. In conclusion, non-hypertensive subjects with a positive family histo ry of hypertension are characterized by a lower activity of the renin- angiotensin-aldosterone system at baseline and a diminished PRa. respo nse during hyperinsulinemia compared with normotensive individuals wit hout such heredity. Whether this is due to volume expansion or to a te ndency to a higher blood pressure remains to be clarified.