The effects of adrenomedullin (AM) and proadrenomedullin N-terminal 20 peptide (PAMP) on membrane potential and sympathetic neurotransmission were studied in rat mesenteric arteries by using microelectrodes. AM (10-7 M) but not PAMP (10-6 M) produced membrane hyperpolarization, which was abolished by high K solution or by glibenclamide, an ATP-sensitive K+ (KATP) channel blocker. Neither AM nor PAMP affected excitatory junction potentials, a measure of sympathetic, purinergic neurotransmission. These findings suggest that AM hyperpolarizes the membrane via activation of KATP channels, which may contribute to the vasodilatory action of AM, whereas the mechanisms of the vasodepressor action of PAMP remain unclear. Copyright (C) 2000 Elsevier Science Inc.
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