Attenuating effects of intrathecal clonidine on the exercise pressor reflex

We tested the hypothesis that intrathecal injection of clonidine, an α₂-adrenergic agonist, attenuated the reflex cardiovascular and ventilatory responses to static muscular contraction in cats. Before clonidine (1 μg in 0.2 ml), contraction-induced reflex increases (n = 10) in mean arterial pressure and ventilation averaged 25 ± 3 mmHg and 359 ± 105 ml/min, respectively, whereas after clonidine these increases averaged 8 ± 4 mmHg and 200 ± 114 ml/min, respectively (P < 0.05). Clonidine had no effect on the heart rate response to contraction. Intrathecal injection of yohimbine (10 μg; n = 5), an α₂-adrenergic antagonist, but not prazosin (10 μg; n = 3), an α₁-adrenergic antagonist, prevented the attenuating effects of clonidine on the reflex pressor and ventilatory responses to contraction. Our findings were not due to the spread of clonidine to the medulla, because the reflex pressor and ventilatory responses to contraction were not attenuated by injection of clonidine (1 μg) onto the medulla (n = 3). In addition, our findings were not due to a clonidine-induced withdrawal of sympathetic outflow, because intrathecal injection of clonidine (1 μg) did not attenuate increases in arterial pressure and ventilation evoked by high-intensity electrical stimulation of the cut central end of the sciatic nerve (n = 5). Furthermore, our findings were not due to a local anesthetic action of clonidine, because application of this agent to the dorsal roots had no effect on the discharge of group IV muscle afferents. We conclude that stimulation of α₂-adrenergic receptors in the spinal cord attenuates the reflex pressor and ventilatory responses to static contraction.