Abstract
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 GsMTx4 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, GsMTx4 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 μg of GsMTx4 into the arterial supply of a hindlimb reduced the peak pressor response (control: 15 ± 4, GsMTx4: 5 ± 2 mmHg, P < 0.05, n = 8) and the pressor response at multiple time points throughout the duration of the stretch. GsMTx4 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 GsMTx4 reduced the pressor response only initially during static stretch in decerebrate rats, the present findings suggest that GsMTx4‐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.
Highlights
The exercise pressor reflex is activated when mechanical and metabolic signals arising from within contracting skeletal muscles stimulate the sensory endings of group III and group IV muscle afferents (Mitchell et al 1983)
We found that GsMTx4 had no effect on the time course of the pressor response or the peak pressor response that resulted from the injection of lactic acid (Fig. 3) which is consistent with the notion that GsMTx4 did not have off-target effects on skeletal muscle sensory neurons such as the inhibition of voltage-gated sodium (NaV) channels (Redaelli et al 2010)
We found that GsMTx4 reduced the pressor response throughout the duration of a 30 sec, 1 Hz dynamic stretch protocol in decerebrate rats
Summary
The exercise pressor reflex is activated when mechanical and metabolic signals arising from within contracting skeletal muscles stimulate the sensory endings of group III and group IV muscle afferents (Mitchell et al 1983). Interest has increased in the reflex’s mechanically sensitive component (i.e., the mechanoreflex) This interest has been driven, in part, by findings that mechanoreflex alterations contribute to the exaggerated exercise pressor reflex present in multiple forms of cardiovascular disease (Middlekauff et al 2001, 2004; Smith et al 2005; Leal et al 2008; Muller et al 2012, 2015; Lu et al 2013).
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