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The hyperpolarizing responses were suppressed by \u03b1<jats:sub>2<\/jats:sub>-noradrenergic receptor antagonists, which suggested that the hyperpolarizing responses reflected stimulation of norepinephrine release from sympathetic neurons. Exposure to ANG II enhanced the amplitude and prolonged the duration of noradrenergic inhibitory postsynaptic potentials and suppressed the amplitude of both fast and slow excitatory postsynaptic potentials. The selective ANG II<jats:sub>1<\/jats:sub>receptor (AT<jats:sub>1<\/jats:sub>R) antagonists, ZD-7115 and losartan, but not a selective AT<jats:sub>2<\/jats:sub>R antagonist (PD-123319), suppressed the actions of ANG II. Western blot analysis and RT-PCR confirmed expression of AT<jats:sub>1<\/jats:sub>R protein and the mRNA transcript for the AT<jats:sub>1<\/jats:sub>R in the enteric nervous system. No expression of AT<jats:sub>2<\/jats:sub>R protein or mRNA was found. Immunoreactivity for AT<jats:sub>1<\/jats:sub>R was expressed by the majority of neurons in the gastric antrum and small and large intestine. AT<jats:sub>1<\/jats:sub>R immunoreactivity was coexpressed with calbindin, choline acetyltransferase, calretinin, neuropeptide Y, and nitric oxide synthase in subpopulations of neurons. The results suggest that formation of ANG II might have paracrine-like actions in the enteric nervous system, which include alterations in neuronal excitability and facilitated release of norepinephrine from sympathetic postganglionic axons. 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