The significance of a sympathetic efferent nerve supply, vasoconstrictor to the carotid body and hence facilitatory to carotid chemoreceptors, is well understood. The significance of a second efferent pathway, whose impulses, passing down the sinus nerve, are inhibitory to the chemoreceptors, is less certain. Activity in these sinus nerve efferents is increased by injection of pressor agents, by hypoxia, by hypercapnia, by application of alkaline solutions to the ventral medulla, and by severe hypocapnia. All these stimuli appear to act centrally. Sinus nerve efferents can also be activated reflexly by stimulating ipsilateral carotid chemoreceptors. The mechanism of efferent inhibition is disputed. A purely cholinergic vasodilator role is unlikely because inhibitory effects are abolished by α-adrenergic antagonists. Since efferents probably cause release of an inhibitory transmitter, dopamine, but convincing evidence for a releasing mechanism has yet to be obtained. Stimulation of nociceptive endings in the heart has reciprocal effects on sinus nerve efferents and sympathetic efferents to the carotid body, inhibiting the former and stimulating the latter. Recent results are cited which indicate that the responses of sinus nerve efferents to changes in blood pressure are more variable than is generally believed, and that the conventional explanation of the relationship between sinus efferent activity and arterial pressure needs to be revised.
|Original language||English (US)|
|Number of pages||6|
|State||Published - 1980|
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