Abstract
To elucidate the role of Ca2+-activated K+ channels in the in vivo catecholamine release from adrenal gland, we implanted microdialysis probes in the left adrenal medulla of anesthetized rats and investigated the effects of high-conductance (BKCa) and low-conductance (SKCa) Ca2+-activated K+ channel antagonists on ACh release from pre-ganglionic splanchnic nerve endings and norepinephrine (NE) and epinephrine (Epi) releases from chromaffin cells. The dialysis probes were perfused with Ringer’s solution containing a cholinesterase inhibitor, neostigmine (10 μM). The left splanchnic nerves were cut and the distal ends were electrically stimulated at 2 and 4 Hz before and after local administration of Ca2+-activated K+ channel antagonists via dialysis probe. Before nerve stimulation basal NE and Epi releases were detected, but ACh release was not detected. BKCa-channel antagonists, iberiotoxin (1 μM, n = 7) and paxilline (100 μM, n = 7) increased basal Epi release and enhanced ACh, NE, and Epi releases induced by nerve stimulation at 2 and 4 Hz. On the other hand, SKCa-channel antagonists, apamine (10 μM, n = 7) and scyllatoxin (2 μM, n = 7) increased basal Epi release and enhanced Epi release induced by nerve stimulation at 2 and 4 Hz, but did not change ACh and NE releases induced by nerve stimulation at 2 and 4 Hz. These data suggest that BKCa-channels regulate ACh release on pre-ganglionic splanchnic nerve endings while SKCa-channels do not, and SKCa-channels regulate Epi release on chromaffin cells. [Jpn J Physiol 55 Suppl:S189 (2005)]
