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Antenatal Exposure to Hypoxia Results in Increased Endothelial Nitric Oxide Synthase (eNOS) in the Rat Carotid Body (CB) ♦ 253

Rat carotid bodies contain eNOS which is postulated to contribute to CB inhibition in response to hypoxia. We hypothesised that chronic antenatal hypoxia would cause an elevation of this inhibitory enzyme. Three rat dams were exposed to 21% O2 (control) and three to 12% O2 (chronic hypoxia) beginning in the midsecond trimester (10 days prior to delivery). No dam delivered prematurely. There were no abortuses or stillbirths and no pups had congenital malformations. The exposures were continued postnatally. On postnatal days 2 and 6, pups (n=31) were weighed sacrificed, and the carotid bodies excised. CB tissue levels of eNOS were analyzed by quantitative immunofluorescent histochemistry. Body weights were lower and growth was attenuated in the hypoxic animals (p<0.05). On day 2, eNOS levels in the hypoxic animals were significantly higher than in controls by an average of 126% (p=0.007). While eNOS levels declined in the hypoxic animals by day 6, they remained elevated above control by an average of 34% (p=.005). We conclude that antenatal hypoxia results in enhanced inhibition of the carotid chemoreceptors through upregulation of eNOS. This enzyme may act both intra- and extravascularly on the chemoreceptor mechanism to limit the carotid afferent activity in response to hypoxia.