Stimulus-secretion coupling in the rat carotid body

• Main Author: Shaw, Karen
• Published: University of Leicester 1989
• Subjects: 572; Biochemistry
• Online Access: http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.254740

The effects of a variety of agents known to stimulate chemoafferent activity were employed to define in greater detail the stimulus-secretion coupling mechanism in the rat carotid body superfused in vitro. Hypoxia, carbachol and sodium cyanide were independently able to elicit amine release. Hypoxia-evoked release was calcium dependent and was reduced by nitrendipine suggesting the involvement of voltage-dependent calcium channels in the secretory response. The effect of carbachol on catecholamine release was abolished by atropine indicating the presence of muscarinic cholinergic receptors on the Type I cells. Hypoxia-induced catecholamine release was partially blocked by atropine suggesting a possible role for muscarinic receptors in the secretory response. Hypoxia, carbachol and cyanide stimulated the release of 4 5Ca from carotid bodies pre-loaded with 4 5Ca, and the release of 4 5Ca by hypoxia or carbachol could be reduced by atropine and nitrendipine. These results suggest that the mobilization of intracellular calcium pools may also contribute to the secretory response. Carbachol was able to stimulate the efflux of [3H] inositol from pre-loaded carotid bodies and the response was abolished in the presence of atropine or lithium. Cytoplasmic concentrations of IP3 and IP3 significantly increased following stimulation with carbachol and the effect was abolished with atropine. In comparison, hypoxia was unable to induce [3H] inositol efflux and only had a moderate effect on inositol phosphate accumulation. These results suggest that carbachol may control cytosolic calcium via the formation of inositol phosphate second messengers. It is suggested that carbachol and hypoxia stimulate catecholamine secretion by altering the intracellular free calcium concentration in the Type I cells. The major effect of hypoxia was to stimulate the entry of extracellular calcium via the voltage-dependent calcium channels whereas mobilization of intracellular calcium stores was a more important event during carbachol-induced catecholamine secretion.