Role of K1 channels in adrenal catecholamine secretion in anesthetized dogs

Nagayama, Takahiro, Kimiya Masada, Makoto Yoshida, Mizue Suzuki-Kusaba, Hiroaki Hisa, Tomohiko Kimura, and Susumu Satoh. Role of K1 channels in adrenal catecholamine secretion in anesthetized dogs. Am. J. Physiol. 274 (Regulatory Integrative Comp. Physiol. 43): R1125–R1130, 1998.—We examined the role of K1 channels in the secretion of adrenal catecholamine (CA) in response to splanchnic nerve stimulation (SNS), acetylcholine (ACh), 1,1-dimethyl-4-phenyl-piperazinium (DMPP), and muscarine in anesthetized dogs. K1 channel blockers and the cholinergic agonists were infused and injected, respectively, into the adrenal gland. The voltage-dependent K1 channel (KA type) blocker mast cell degranulating (MCD) peptide infusion (10–100 ng/min) enhanced increases in CA output induced by SNS (1–3 Hz), but it did not affect increases in CA output induced by ACh (0.75–3 μg), DMPP (0.1–0.4 μg), or muscarine (0.5–2 μg). The small-conductance Ca21-activated K1 (SKCa) channel blocker scyllatoxin infusion (10–100 ng/min) enhanced the ACh-, DMPP-, and muscarine-induced increases in CA output, but it did not affect the SNS-induced increases in CA output. These results suggest that KA channels may play an inhibitory role in the regulation of adrenal CA secretion in response to SNS and that SKCa channels may play the same role in the secretion in response to exogenously applied cholinergic agonists.