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The hypoxic stimulus of arterial blood is transformed at the carotid body (CB) chemoreceptors into neuronal signals regulating respiration.The mechanism of chemotransduction is until now not well understood.In this study the regulation of arachidonic acid (AA) release and its incorporation into membrane glycerolipids were investigated.Moreover, the effect of hypoxia and dopamine (DA) on these processes was calculated.The CB were excised from cats exposed in situ to normoxia or hypoxia.Then CB were homogeni and used as a source of enzyme (s).It was observed thar Ca2+ enhanced the release of AA by 40-50% through the action of phospholipase C together with diacyl-glycerol lipase and phospholipase A2.Acute hypoxia significantly decreased AA incorporation into phosphatidylinositol (PtdIns) and enhanced the level of AA radioactivity in diacylglycerol and AA-CoA.These results suggest that hypoxia induces inhibition of AA on the level of acyl-CoA-lysophospholipid:acylotransferases.DA decreased AA incorporation into PtdIns and exerted an additive inhibitory effect in hypoxic samples.These results demonstrated that AA metabolism in CB is significantly affected by hypoxia and that DA is not responsible for the hypoxia-induced alteration of lipid metabolism in CB.
2
Content available remote NADPH-diaphorase in the cat carotid body
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Ultrastructural examinations of the CB showed that NOS-related NADPH-d activity is present in the chemoreceptor cells (Fig. 1A). The NADPH-d reaction product appeared as small, intense, dark particles scattered in the cytoplasm of the cells. The particles were distributed most densely or tended to aggregate in the perinuclear region, the endoplasmic reticulum channels, and in between the dense-core vesicles but not in the vesicles themselves. These particles were distinguishable from ribosomes from which they were larger and more electron dense. The particles were absent in the control specimens in which B-NADPH was omitted (Fig. 1B). The presence of NOS, which synthesizes a short-lived gaseous NO messenger, may have significant implications for the CB function. NO could not only affect the autonomic and sensory nerve endings but also be a direct participant of the chemoreceptor cell signaling process. The exact role of the nitergic pathway in the CB is unclear at present.
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