Chronic hypoxia upregulates the expression and function of AT(1) receptor in rat carotid body

In the present study, the effects of chronic hypoxia on the expression and localization of angiotensin II (Ang II) receptors are investigated by semi- quantitative reverse transcription-polymerase chain reaction (RT-PCR) and b y immunohistochemistry. The effect of chronic hyper-in on the carotid body chemoreceptor activity was also examined by in vitro electrophysiology. Res ults from RT-PCR revealed that chronic hypoxia exhibited differential effec ts on the gene expression of Ang II receptors, namely AT(1) and AT(2), in t he carotid body. The mRNA expression for subtypes of the AT(1) receptor, AT (1a) and AT(1b), was significantly increased in the carotid body with chron ic hypoxia. To further investigate the localization of the AT(1) receptor, an immunohistochemical study was performed. The results showed that AT(1) r eceptor immunoreactivity was found in lobules of glomus cells in the caroti d body and the immunoreactivity was more intense in chronic hypoxia than in normoxic controls. In vitro electrophysiological studies consistently demo nstrated that chronic hypoxia enhanced the AT(1) receptor-mediated excitati on of carotid body chemoreceptor activity. These data suggest that chronic hypoxia upregulates the transcriptional and post-transcriptional expression of AT(1) receptors in the rat carotid body. The upregulation of the expres sion also enhances AT(1) receptor-mediated excitation of the carotid body a fferent activity. This might be important in the modulation of cardiorespir atory functions as well as fluid and electrolyte homeostasis during chronic hypoxia.