Integrated carotid chemoreceptor and pulmonary inflation reflex control of peripheral vasoactivity in conscious dogs.

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Abstract
The interaction of carotid chemoreceptor and pulmonary inflation reflex control of vascular responses in the mesenteric, renal and iliac beds was examined in conscious dogs by comparing responses to chemoreceptor stimulation (intracarotid injection of nicotine or cyanide) during spontaneous and controlled respiration. A biphasic response was evoked which was characterized by initial bradycardia, increase in mean arterial pressure, and marked increase in resistance in the iliac [102 .+-. 17% (mean .+-. SE)] as compared with the mesenteric (16 .+-. 3%) and renal (9 .+-. 2%) beds. After the chemoreceptor-induced increases in ventilation, there was a later phase characterized by tachycardia, a decrease in mean arterial pressure and a striking decrease in resistance in the iliac (-51 .+-. 2%) as compared with the mesenteric (-3 .+-. 4%) and renal (-11 .+-. 3%) beds. .alpha.-Blockade with phentolamine nearly abolished the early vasoconstriction and later vasodilation. When the chemoreceptor-induced increase in respiration was prevented, or after bilateral vagotomy, there was significantly more (P < 0.01) vasoconstriction in all 3 beds and no later vasodilation. After mechanical hyperinflation of the lungs, a striking decrease in resistance was observed in the iliac (-56 .+-. 3%) as compared with the mesenteric (-17 .+-. 5%) and renal (-6 .+-. 6%) beds; these responses were not observed after .alpha.-blockade or after vagotomy. Responses to carotid chemoreceptor stimulation were not observed after carotid sinus nerve section. Carotid chemoreceptor stimulation in conscious dogs with spontaneous respiration results in a biphasic vascular response. Pulmonary inflation reflexes attenuate the initial vasoconstrictor response to carotid chemoreceptor stimulation and are responsible for the later period of vasodilation.