Acute hypoxia modulates arachidonic acid metabolism in cat carotid bodies. Role of dopamine

Abstract

The hypoxic stimulus of the 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 evaluated. The CB were excised from cats exposed in situ to normoxia or hypoxia. Then CB were homogenized and used as a source of enzyme (s). It was observed that Ca2+ enhanced the release of AA by 40–50% through the action of phospholipase C together with diacyl-glycerollipase 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 incorporation 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 demonstrate 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.