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Ionic Mechanisms of the Chemoreception Process in Type 1 Cells of the Carotid Body
Año del Documento
Arterial Chemoreception. New York, 1990, p. 44-57
Tbe receptor complex in the carotid body (CB) is formed by clusters of type 1 cells that are connected synaptically to the endings of the chemo sensory fibers of the carotid sinus nerve (CSN), partia lly covered by type JI cells, and surrounded by a dense net of fenestrated capillaries (1). Sorne aspects of CB chemoreceptor physiology such as the identity of adequate stimulus, the characteristics of the receptor response to the dif ferent stimuli, and the reflex responses elicited upon CB stimulation are well known. Contrary to this, the basic mechanisms operating in this re ceptor are not completely understood (2). It has been proposed that low Po2 will decrease the ATP leveIs in the chemoreceptor or type 1cells and that this decrease in ATP will trigger the release of neurotransm itters capable of activating the sensory nerve endings. However, there is no proposal on how the decrease in ATP levels can activate the release process. It has been proposed also that high Pco2 and/or low pH in blood will increase the intracellular H+ concentration and that it will result i n in creased intracellu lar Ca2 + in type 1 cells and in the release of transmitters. Once again , there is no proposal on the mechanisms by which the increase in H+ can produce the increased Ca2+ concentration in type I cells (2,3).
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