Role of K⁺ channels in adrenal catecholamine secretion in anesthetized dogs

We examined the role of K⁺ channels in the secretion of adrenal catecholamine (CA) in response to 4 splanchnic nerve stimulation (SNS), acetylcholine (ACh), 1,1-dimethyl-4-phenyl-piperazinium (DMPP), and muscarine in anesthetized dogs. K⁺ channel blockers and the cholinergic agonists were infused and injected, respectively, into the adrenal gland. The voltage- dependent K⁺ channel (K(A) 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 Ca²⁺-activated K⁺ (SK(Ca)) 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 K(A) channels may play an inhibitory role in the regulation of adrenal CA secretion in response to SNS and that SK(Ca) channels may play the same role in the secretion in response to exogenously applied cholinergic agonists.