Journal of Applied Physiology, Vol 68, Issue 5 1844-1849, Copyright © 1990 by American Physiological Society
Cobalt stimulates carotid body chemoreceptors
C. Di Giulio, W. X. Huang, S. Lahiri, A. Mokashi and D. G. Buerk
Department of Physiology, University of Pennsylvania School of Medicine, Philadelphia.
Because cobalt administration is known to elicit erythropoietin response,
it is a reasonable hypothesis that cobalt would also stimulate the
O2-sensing process in the peripheral chemoreceptors. We tested this
hypothesis by measuring the effects of cobalt chloride on carotid
chemosensory fibers in pentobarbital-anesthetized cats that were paralyzed
and artificially ventilated. Responses of carotid chemoreceptor afferents
to graded doses of cobalt given by intra-arterial injections (0.08-2.10
mumols) were measured at constant blood gases. Responses of the same
chemoreceptor afferents to hypoxia, before and after a saturation dose of
cobalt, were measured. In two experiments carotid body tissue PO2 was also
simultaneously measured. The chemosensory fibers showed prolonged
excitation after a brief period of inhibition subsequent to cobalt
administration. The stimulatory effect showed a dose-dependent saturation
response. Cobalt augmented rather than blocked carotid chemoreceptor
response to hypoxia. The effect of cobalt was not mediated by tissue PO2.
These results are consistent with the hypothesis that cobalt stimulates the
O2-sensing mechanism, although a direct effect of cobalt on the
excitability of the chemosensory terminal remains a possibility.
