Chronic cobalt causes hypertrophy of glomus cells in the rat carotid body.
We tested the hypothesis that chronic cobalt administration would induce carotid body cellular response along with polycythemia as found in chronic hypoxia if common oxygen-sensitive mechanisms were involved in the two instances. Morphometric studies were performed on carotid bodies in male rats that were chronically treated with cobalt chloride (0.17 mumol/kg, ip, daily for 6 wk) and in control rats that received blank saline injections. The rats were anesthetized, blood samples were collected for hematocrit, and the carotid bodies were surgically exposed and were perfused and superfused with the buffered fixative (3% glutaraldehyde plus 1% paraformaldehyde, pH 7.40, 330-340 mosM). The carotid bodies were processed, and ultrathin sections were cut for electron microscopy and morphometry of type I (glomus) and type II cells. Hematocrit increased from 44% in the control to 74% in the cobalt-treated rats, and the mean volume of type I cells increased from 424 to 1,061 microns 3. Type II cells did not show any significant change in size. The results suggest that cobalt stimulated oxygen-sensitive mechanism in the glomus cells of the carotid body and that the glomus cell is a site of oxygen chemosensing.
Di Giulio
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Department of Physiology, University of Pennsylvania School of Medicine, Philadelphia 19104-6085.
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Lahiri
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D000818:Animals; D002344:Carotid Body / Q000187:drug effects* / Q000473:pathology; D003035:Cobalt / Q000633:toxicity*; D004920:Erythropoiesis / Q000187:drug effects; D006400:Hematocrit; D006984:Hypertrophy / Q000139:chemically induced; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains
D003035:Cobalt; C018021:cobaltous chloride