Evidence is presented which indicates that in the absence of other known inputs to the nervous system and during controlled pulmonary ventilation, stimulation of the carotid body chemoreceptors causes bradycardia and selective peripheral vasoconstriction. These responses may be attenuated, however, by concomitant changes in respiration and arterial blood pressure, and by activity of higher parts of the brain stem. Stimulation of the aortic bodies in mammals in which they are functionally active, causes bradycardia or tachycardia and selective peripheral vasoconstriction. The reflex vascular effects from the peripheral arterial chemoreceptors are mediated by alpha-adrenergic sympathetic fibres. A potential mechanism exists therefore whereby the peripheral arterial chemoreceptors could contribute to the neurogenic component of hypertension.