Abstract
Summary
The vascular responses in the hind paw associated with stimulation of the carotid body chemoreceptor reflex were studied in morphine-sedated, chloralose-urethane-anesthetized dogs. Intracarotid arterial injection of nicotine (30-200 μg) elicited reflex vasodilatation in the perfused hind paw in control animals. In animals treated for 3 consecutive days with guan-ethidine (2.5, 5, and 5 mg/kg/day) chemoreceptor stimulation with nicotine failed to evoke reflex vasodilatation in the hind paw, whereas intraarterial administration of ni-troglycerin and stimulation of the intact tibial nerve readily produced vasodilatation. Acute administration of guanethidine (5 mg/kg) also abolished chemoreceptor reflex-induced responses in the hind paw. The results of this investigation suggest that the chemoreceptor reflex-induced vasodilatation in the hind paw is due to an inhibition of sympathetic vasoconstrictor tone and does not represent activation of sustained vasodilatation.
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