Carotid Chemosensory Stimulation by Sulfhydryls and Almitrine is not Mediated by Tissue Hypoxia
One hypothesis for carotid body chemoreception postulates that there is a plasma membrane protein which reversibly binds with O2 similar to myoglobin or hemoglobin (Lloyd et al., 1968; Lahiri and DeLaney, 1975). Protein conformation changes with O2, CO2, pH or other chemical species could regulate K+ or other ion channels. Lahiri (1981) found that the alkylating agent N-ethylmaleimide (NEM) stimulated carotid receptors and augmented hypoxic responses, and suggested that a protein containing sulf-hydryl groups located in carotid body cell membranes might have mediated the responses. Almitrine bismesylate is another pharmacological agent which stimulates carotid chemoreceptors (Laubie and Schmitt, 1980) and also alters whole body sodium and water regulation (Honig, 1989). Lahiri et al. (1989) recently demonstrated that almitrine lowers the stimulus threshold and augments the response to CO2 apparently without affecting O2 sensing mechanisms. However, it has not been confirmed whether NEM or almitrine alter chemoreception directly, or indirectly by increasing carotid body O2 metabolism or by constricting blood flow, thereby lowering tissue PO2.
KeywordsCarotid Body Carotid Sinus Nerve Arterial Chemoreceptor Carotid Chemoreceptor Carotid Body Chemoreception
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