Low‐dose aspirin augments carotid‐cardiac baroreflex sensitivity during concurrent muscle mechanoreflex and metaboreflex activation in humans

Abstract

Metabolite sensitization of muscle mechanoreceptors alters carotid baroreflex (CBR) sensitivity but the role of thromboxane (TX) A2 is unknown. Therefore, we examined the effect of inhibiting TX A2 via low‐dose aspirin on carotid‐cardiac (CBR‐HR) and carotid‐vasomotor (CBR‐MAP) sensitivity during mechanoreflex and metaboreflex activation in humans. 9 subjects performed 1.5mins of 70% MVC isometric calf exercise, 3.5mins of post‐exercise circulatory occlusion, then 3mins of occlusion plus passive calf stretch. This occurred twice after 7 days of either low‐dose aspirin (Asp) or placebo (Pla). Asp reduced baseline TX B2 by ~90% (p<0.05). Maximal gains at rest were similar in all trials for CBR‐HR and CBR‐MAP (−0.44±0.1 vs. −0.37±0.1 b.min−1.mmHg−1 and − 0.23±0.0 vs. −0.20±0.0 mmHg.mmHg−1 for Asp and Pla, respectively). CBR‐HR maximal gain during stretch with Asp was significantly higher than with Pla (−0.64±0.1 vs. −0.33±0.1 b.min− 1.mmHg−1, respectively) (p<0.05). CBR‐MAP maximal gain during stretch with Asp was similar to with Pla (−0.29±0.0 vs. −0.33±0.1 mmHg.mmHg−1, respectively). These results suggest that low‐dose Asp augments CBR‐HR but not CBR‐MAP sensitivity during concurrent mechanoreflex and metaboreflex activation in humans. This could be due to increased cardiac vagal activity caused by reduced TX sensitization of mechanoreceptors. Supported by P01 HL096570 (LIS); UL1 RR033184 (LIS).