Zusammenfassung

We investigated the contribution of tetrodotoxin (TTX)-resistant sodium channels to the augmented exercise pressor reflex observed in decerebrated rats with femoral artery ligation. The pressor responses to static contraction, to tendon stretch, and to electrical stimulation of the tibial nerve were compared before and after blocking TTX-sensitive sodium channels on the L3-L6 dorsal roots of rats whose hindlimbs were freely perfused and rats whose femoral arteries were ligated 72 h before the start of the experiment. In the freely perfused group (n = 9), pressor (Δ22 ± 4 mmHg) and cardioaccelerator (Δ32 ± 6 beats/min) responses to contraction were attenuated by 1 μM TTX (Δ4 ± 1 mmHg, P < 0.05 and Δ17 ± 4 beats/min, P < 0.05, respectively). In the 72 h ligated group (n = 9), the augmented pressor response to contraction (32 ± 4 mmHg) was also attenuated by 1 μM TTX (Δ8 ± 2 mmHg, P < 0.05). The cardioaccelerator response to contraction was not significantly attenuated in these rats. In addition, TTX suppressed the pressor response to tendon stretch in both groups of rats. Electrical stimulation of the tibial nerve evoked similar pressor responses between the two groups (freely perfused: Δ74 ± 9 mmHg and 72 h ligated: Δ78 ± 5 mmHg). TTX attenuated the pressor response to the tibial nerve stimulation by about one-half in both groups. Application of the TTX-resistant sodium channel blocker A-803467 (1 μM) with TTX (1 μM) did not block the pressor response to tibial nerve stimulation to any greater extent than did application of TTX (1 μM) alone. Although the contribution of TTX-resistant sodium channels to the augmented exercise pressor reflex may be slightly increased in rats with chronic femoral artery ligation, TTX-resistant sodium channels on dorsal roots do not play a major role in the augmented exercise pressor reflex.