Abstract

Increasing evidence indicates that angiotensin (Ang) II ‐induced outward potassium current (Ik) inhibition in the carotid body (CB) enhances CB chemoreceptor sensitivity. ACE2 has been identified as a critical negative modulator of Ang II bioactivity, counterbalancing the effects of ACE in determining net tissue Ang II levels. This, coupled with the knowledge that ACE2 is a key enzyme in the formation of Ang 1‐7, led us to hypothesize that Ang 1‐7 would oppose Ang II‐induced Ik inhibition in the CB. Immuno blot analysis confirmed that ACE2 and Mas receptor (Ang 1‐7 receptor) protein are expressed in the rabbit CB. Ang 1‐7 (50 nM) enhanced Ik in CB glomus cells by 16 ± 4%. The Mas receptor antagonist A779 (1 μM) inhibited the effects of Ang 1‐7. Ang II (100 nM) reduced Ik by 91 ± 5%. However, in the presence of Ang 1‐7 (50 nM), AngII reduced Ik by only 12 ± 2%. Hypoxia (PO2=40 Torr)‐induced Ik inhibition (24 ± 4%) was also blunted by Ang 1‐7 (10±3%, P <0.05 versus hypoxia alone) in the CB glomus cells. Together, these findings indicate that Ang 1‐7 attenuates the action of Ang II, which might be involved in the regulation of the CB chemoreceptor sensitivity. (NIH PO1‐HL62222)

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