Gs MT x4 reduces the reflex pressor response during dynamic hindlimb skeletal muscle stretch in decerebrate rats

Mechanical signals within contracting skeletal muscles contribute to the generation of the exercise pressor reflex; an important autonomic and cardiovascular control mechanism. In decerebrate rats, the mechanically activated channel inhibitor Gs MT x4 was found to reduce the pressor response during static hindlimb muscle stretch; a maneuver used to investigate specifically the mechanical component of the exercise pressor reflex (i.e., the mechanoreflex). However, the effect was found only during the initial phase of the stretch when muscle length was changing and not during the later phase of stretch when muscle length was relatively constant. We tested the hypothesis that in decerebrate, unanesthetized rats, Gs MT x4 would reduce the pressor response throughout the duration of a 30 sec, 1 Hz dynamic hindlimb muscle stretch protocol that produced repetitive changes in muscle length. We found that the injection of 10  μ g of Gs MT x4 into the arterial supply of a hindlimb reduced the peak pressor response (control: 15 ± 4, Gs MT x4: 5 ± 2 mmHg, P  < 0.05, n  = 8) and the pressor response at multiple time points throughout the duration of the stretch. Gs MT x4 had no effect on the pressor response to the hindlimb arterial injection of lactic acid which indicates the lack of local off‐target effects. Combined with the recent finding that Gs MT x4 reduced the pressor response only initially during static stretch in decerebrate rats, the present findings suggest that Gs MT x4‐sensitive channels respond primarily to mechanical signals associated with changes in muscle length. The findings add to our currently limited understanding of the channels that contribute to the activation of the mechanoreflex.