Abstract
The carotid body (CB) is a polymodal peripheral chemoreceptor that registers the levels of pO2, pCO2 and pH in the arterial blood, and maintains homeostatic regulation in the respiratory and cardiovascular systems. The aim of the present study was to create an animal model for investigating the effects of acute nitrite treatment on the CB morphology in rats. Chemical hypoxia was induced by a single intraperitoneal injection of sodium nitrite (50 mg/kg). Using hematoxylin and eosin-stained sections we studied the morphological changes in the Wistar rat CB induced by hemic hypoxia in comparison with the control normoxic CB. The present data show that a single injection of sodium nitrite causes the development of marked structural alterations in the rat CB. We observed that 1 h after the administration, the CB underwent structural changes characterized by a prominent increase in its size with a marked several-fold dilation of the blood vessels. The obvious CB enlargement was at its highest one day later and persisted until the 5th day after the sodium nitrite injection, and then slowly decreased in the days to follow. Interestingly, 20 days following the treatment the expanded CB vasculature in nitrite-injected animals returned to the normoxic control state, although its size remained somewhat larger. Morphometric analysis revealed that the CB size increase in treated animals was statistically significant when compared to that of untreated controls. In conclusion, we demonstrate that acute treatment with sodium nitrite causes statistically significant enlargement of the CB and a pronounced vasodilation. It can be inferred that the nitrite-exposed CB displays remarkable structural plasticity and increases its size mostly through vascular expansion.
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