Interaction between sodium intake, angiotensin II, and blood pressure as a cause of cardiac hypertrophy.

Cardiac hypertrophy is common in hypertension but its development is influenced by angiotensin II, sodium intake aldosterone, and the time of day blood pressure (BP) is elevated. This study examined and compared cardiac hypertrophy in the 2 kidney-1 clip (2K-1C) and 1 kidney-clip (1K-1C) Goldblatt models of hypertension. Blood pressure was measured by telemetry in a selected group of rats. Rats were placed on a high (4%) or reduced (0.2%) salt intake and were given captopril (75 mg/kg per day) or losartan (10 mg/kg per day). Appropriate sham-operated and untreated controls were used. Cardiac hypertrophy was greater in the IK-1C than in the 2K-1C model. Day and sleep BP were also higher. In the 2K-1C model BP was lower on the reduced salt intake and BP decreased with captopril in both reduced and high salt groups. Cardiac weight and index decreased significantly only in the reduced salt and captopril group and was less than the size before treatment. In the 1K-1C model captopril caused all BP measures to decrease in the reduced salt group but had no significant effect in the high salt group. Cardiac weight and index were reduced only in the reduced salt + captopril group and cardiac weight was less than the pretreatment control. Losartan had a similar effect in the lK-1C model to that achieved with captopril. The responses achieved correlated in part with renin status and dependency level. There is no prime determinant of cardiac hypertrophy. Blood pressure, sodium intake, and hormonal status are all important. It is postulated that the common pathway may be alterations in cell composition that signal the nucleus to increase cell growth.