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Angiotensin II Evokes Sensory Long‐Term Facilitation of the Carotid Body
Author(s) -
Peng YingJie,
Kumar Ganesh,
Prabhakar Nanduri
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.669.9
In the present study we examined the effects of excitatory transmitters/modulators for their ability to evoke sensory long‐term facilitation (sLTF) of the carotid body. Sensory activity was recorded from ex vivo carotid bodies harvested from adult rats. Carotid bodies were challenged with 5 applications (30s challenge separated by 5min) of one of the following subtances: Acetyl choline (ACh;10μM), ATP (100μM), Substance P (SP;1μM), Endothelin‐1(ET‐1;50nM), Angiotensin II (AngII; 300pM) and KCl (40 mM). Baseline sensory activity was monitored before, during and for 60 min after the five challenges with each of the above agents. Among the substances tested, only Ang II elicited sLTF of the carotid body. Ang II‐evoked sLTF was prevented by AT‐1 receptor antagonist, losartan (3μM) or NADPH oxidase (Nox) inhibitors apocynin (500μM) or AEBSF (500μM). Ang II increased Nox‐dependent ROS generation in the carotid body. Ang II‐evoked sLTF was absent in mice deficient in Nox2. These observations demonstrate that AngII evokes sLTF of the carotid body via Nox activation by AT‐1 receptors. Supported by NIH ‐HL‐76537, HL‐90554.