Role of blood pressure in chronic aldosterone‐mediated cardiac injury (701.5)

Abstract

Excess aldosterone (ALDO) causes hypertension (HTN), and cardiac hypertrophy, injury and dysfunction. The role of HTN in ALDO‐mediated cardiac injury remains controversial. We aim to study the role of blood pressure (BP) in chronic ALDO‐mediated cardiac hypertrophy and fibrosis.Eight‐week old uninephrectomized male Sprague Dawley rats (N=6/grp) were implanted with radiotelemetry probes for BP monitoring and allowed to recover for 2 wks. Animals were assigned to 4 groups: Control, ALDO (0.75 µg/h)/SALT (1.0 % NaCl + 0.3 % KCl in drinking water), ALDO/SALT+2‐AHT (240 mg/kg hydralazine and 15 mg/kg reserpine in the food) or ALDO/SALT+3‐AHT (2‐AHT plus 75 mg/kg hydrochlorothiazide). Tissue weights and cardiac fibrosis were determined at the end of the 8‐week experimental period.All three ALDO‐treated groups reached the same BP value at the end of the 8‐wk period. However, the MAP area under the curve (AUC) was decreased in 2‐AHT (1.47 AU vs. ALDO, p<0.05; vs. 3‐AHT, p<0.05) and 3‐AHT (1.29 AU vs. ALDO, p<0.0.5) vs. ALDO (1.73 AU vs. control, p<0.05). Cardiac fibrosis positively correlated with MAP AUC (R2=0.51, p<0.05) as well as with heart, left ventricle, kidney and lung weights.These results suggest that ALDO‐mediated cardiac hypertrophy and fibrosis is BP‐dependent without excluding that ALDO may exacerbate the HTN‐mediated cardiac injury. Stricter BP management may benefit patients with elevated ALDO levels.Grant Funding Source: Supported by American Heart Association Grant 12SDG8980032.