Blood pressure reactivity to emotional stress is reduced in AT1A-receptor knockout mice on normal, but not high salt intake.

Pharmacological evidence suggests that angiotensin II type 1 (AT(1)) receptors are involved in the regulation of cardiovascular response to emotional stress and reinforcing effect of dietary salt on this response. In this study, we examined the effect of genetic deletion of AT(1A) receptors on the cardiovascular effects of stress and salt in mice. AT(1A) receptor knockout (AT(1A)(-/-)) and wild-type (AT(1A)(+/+)) mice were implanted with telemetry devices and placed on a normal (0.4%) or high (3.1%) salt diet (HSD). Resting blood pressure (BP) in AT(1A)(-/-) mice (84+/-3 mm Hg) was lower than in AT(1A)(+/+) mice (107+/-2 mm Hg). Negative emotional (restraint) stress increased BP by 33+/-3 mm Hg in AT(1A)(+/+) mice. This response was attenuated by 40% in AT(1A)(-/-) mice (18+/-3 mm Hg). Conversely, the BP increase caused by food presentation and feeding was similar in AT(1A)(-/-) (25+/-3 mm Hg) and AT(1A)(+/+) mice (26+/-3 mm Hg). HSD increased resting BP by 14+/-4 mm Hg in AT(1A)(-/-) mice without affecting it significantly in AT(1A)(+/+) mice. Under these conditions, the pressor response to restraint stress in AT(1A)(-/-) mice (30+/-3 mm Hg) was no longer different from that in wild-type animals (28+/-3 mm Hg). The BP response to feeding was not altered by HSD in either AT(1A)(-/-) or AT(1A)(+/+) mice (25+/-2 and 27+/-3 mm Hg, respectively). These results indicate that AT(1A) receptor deficiency leads to a reduction in BP reactivity to negative emotional stress, but not feeding. HSD can selectively reinforce the cardiovascular response to negative stress in AT(1A)(-/-) mice. However, there is little interaction between AT(1A) receptors, excess dietary sodium and feeding-induced cardiovascular arousal.