Abstract
Introduction: The carotid body (CB) is a small, paired, neural crest-derived neuroendocrine organ that senses the oxygen level in blood and maintains homeostatic regulation in the respiratory and cardiovascular systems. It has a typical dual innervation by both sensory nerve fibers of the primary afferent neurons located in the petrosal ganglion and by the postganglionic sympathetic nerve fibers from the superior cervical ganglion (SCG). Recent evidence suggests that angiotensin II acting via AT1 receptors modulates the activity of chemical substances in a paracrine-autocrine manner. Aim and Methods: The study aims at investigating the immunohistochemical localization of the AT1 receptor in the CB and SCG of intact rats and after treatment with its selective blocker losartan. Results: We found that a population of the CB glomus cells and the vast majority of closely located SCG neurons were richly endowed with AT1 receptors while the nerve fibers supplying the CB did not express the receptor protein. Our data also revealed that the intensity of immunostaining reverberating receptor protein levels was significantly decreased by losartan. In particular, its administration caused a less dense immunostaining of glomus cells in treated rats compared with the control animals treated with a vehicle. Similarly, the intensity of receptor immunostaining in the SCG neurons after losartan treatment was lower than in the ganglion cells of controls. Conclusion: It can be inferred that angiotensin II acting via AT1 receptor activation is involved in CB excitation under normoxic conditions. Understanding the principles by which AT1 receptor activation amplifies CB chemosensory reactivity to oxygen would provide insights in the pathophysiology of certain hypoxemia-related disorders. Acknowledgments: This work was supported by the Medical University of Sofia, Bulgaria (grant No. 14/2016)
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