Chronic Femoral Artery Ligation Exaggerates the Exercise Pressor Reflex but Not Selective Activation of the Muscle Mechanoreflex in Decerebrate Rats
Authors: Rollins Korynne S , Esau Peter J , Copp Steven W 
Published: November 2023

Mechanical and metabolic stimuli arising within contracting skeletal muscles reflexly increase sympathetic nervous system activity, blood pressure, and heart rate. This reflex, termed the exercise pressor reflex, is exaggerated in a rat model of limb ischemia in which a femoral artery is chronically ligated. We recently found that the mechanically‐sensitive component of the exercise pressor reflex contributes to its exaggeration in rats with a ligated femoral artery despite no difference in mechano‐gated channel protein expression in lumbar dorsal root ganglia (DRG) tissue. This suggests that metabolite‐induced sensitization of mechanoreceptors underlies the exaggerated mechanically‐sensitive component of the exercise pressor reflex in ligated rats. This prompted us to seek the physiological evidence in support of the anatomical evidence that ligation does not increase mechano‐gated channel expression in DRG tissue.

Objective

We used a within‐rat comparison experimental design to test the hypothesis that the increase in blood pressure, heart rate, and renal sympathetic nerve activity (RSNA) during selective activation of the muscle mechanoreflex (a purely mechanical stimulus) would not be different when evoked from a freely perfused hindlimb compared a ligated hindlimb.

Methods

Fifteen male Sprague‐Dawley rats had their left femoral artery ligated 72 hours before the experiment. In decerebrate, unanesthetized rats the muscle mechanoreflex was selectively activated by passively stretching the Achilles tendon for 30 s. In five of those fifteen rats, the exercise pressor reflex was evoked by electrically‐stimulating the sciatic nerves for 30 s which produced static hindlimb muscle contractions.

Results

In 10 rats there were no differences between the peak pressor (freely perfused: 13±2, ligated: 14±3 mmHg, p=0.801), cardioaccelerator (freely perfused: 12±2, ligated: 11±2 bpm, p=0.672), or RSNA (freely perfused: 40±7, ligated: 46±6%, p=0.377) responses evoked by tendon stretch of the freely perfused and ligated hindlimbs. In five additional rats, the exercise pressor reflex was greater when evoked from the contracting ligated hindlimb (28±3 mmHg) compared to the contracting freely perfused hindlimb (21±3 mmHg, p=0.014). In those same five rats, however, in which femoral artery ligation exaggerated the exercise pressor reflex there was no difference in the peak pressor response to tendon stretch between hindlimbs (freely perfused: 16±2, ligated: 15±3 mmHg, p=0.581).

Conclusion

We found that the reflex pressor, cardioaccelerator, and RSNA responses to tendon stretch (a purely mechanical stimulus) were not exaggerated by femoral artery ligation, even in rats in which the exercise pressor reflex was confirmed to be exaggerated by ligation. These findings indicate that the ligation‐induced exaggeration of the mechanically‐sensitive component of the exercise pressor reflex reported previously must be due to a metabolite‐induced sensitization of mechano‐gated receptors.

Support or Funding Information

Departmental funds