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Vascular Biology Center, Departments of Surgery, Physiology, and Pharmacology and Toxicology, Medical College of Georgia, Augusta, Georgia 30912-2500
Recent evidence suggests that endothelin-1 (ET-1), perhaps
through the ETB receptor, may participate in blood pressure
regulation through the control of sodium excretion. Mean arterial
pressure (MAP) was continuously measured via telemetry implants in male Sprague-Dawley rats. After 1 wk of baseline measurements, rats were given either high (10%) or low (0.08%) NaCl in chow for the remainder of the experiment (n = 5 in each group). MAP
was significantly increased in rats on a high-salt diet (115 ± 2 mmHg) compared with rats on the low-salt diet (103 ± 2 mmHg;
P < 0.05). All rats were then treated with the
ETB receptor antagonist A-192621 mixed with the food and
adjusted daily to ensure a dose of 30 mg · kg
1 · day1.
ETB blockade produced an increase in MAP within a few hours of treatment and was significantly higher in rats on the high-salt diet
over a 1-wk period (170 ± 3 vs. 115 ± 3 mmHg,
P < 0.01). To determine whether the increase in MAP
during A-192621 treatment was due to increased ETA receptor
activation, all rats were then given the ETA-selective
antagonist ABT-627 in the drinking water while a low-salt/high-salt
diet and ETB blockade were continued. ABT-627 decreased MAP
within a few hours in rats on either the high-salt (113 ± 3 mmHg)
or low-salt (101 ± 3 mmHg) diet. These results support the
hypothesis that endothelin, through the ETB receptor,
participates in blood pressure regulation in the response to salt loading.
blood pressure; hypertension; water-electrolyte balance
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