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. 1981 Jun;315:81–98. doi: 10.1113/jphysiol.1981.sp013734

Responses of carotid body chemosensory activity and blood flow to stimulation of sympathetic nerves in the cat.

R G O'Regan
PMCID: PMC1249369  PMID: 7310725

Abstract

1. The effects of electrical stimulation of sympathetic nerves on sinus nerve chemosensory activity and carotid body blood flow were investigated in anaesthetized cats. 2. Two categories, designated as types I and II, of excitatory responses of chemosensory discharges to sympathetic stimulation were distinguished. Type I responses displayed elevations in impulse frequencies which were usually maximal in the initial 10-20 sec of stimulation, resisted alpha-adrenoceptor antagonism induced by phentolamine or phenoxybenzamine and were enhanced after administration of the dopamine antagonist, haloperidol. Type II responses showed increases in impulse frequencies which became more pronounced as stimulation progressed. These responses were susceptible to alpha-adrenoceptor blockade, were unaffected by haloperidol administration and were usually recorded during systemic hypotension. 3. Inhibitory changes due to activation of sympathetic fibres were recorded in 10% of chemosensory preparations. These effects were usually either abolished or replaced by type I excitatory responses after haloperidol administration. 4. Sympathetic stimulation caused reductions of carotid body blood flow during both natural and artificial perfusion of the organ. This effect was abolished or considerably attenuated by alpha-adrenoceptor antagonism and was unaffected by haloperidol administration. 5. Possible mechanisms which could account for the influences of sympathetic stimulation on chemoreceptor activity and carotid body blood flow are discussed. It is concluded that inhibitory and type I excitatory responses probably arise from activation of sympathetic fibres with non-vascular terminations within the carotid body. Type II excitatory responses are most likely due to blood flow changes.

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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

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