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Am J Physiol Regul Integr Comp Physiol 274: R1125-R1130, 1998;
0363-6119/98 $5.00
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Vol. 274, Issue 4, R1125-R1130, April 1998

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

Takahiro Nagayama1, Kimiya Masada1, Makoto Yoshida1, Mizue Suzuki-Kusaba1, Hiroaki Hisa1, Tomohiko Kimura2, and Susumu Satoh1

1 Department of Pharmacology, Pharmaceutical Institute, Tohoku University, Aobayama, Sendai 980-77; and 2 Department of Dental Pharmacology, The Nippon Dental University School of Dentistry at Niigata, Niigata 951, Japan

We examined the role of K+ 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. K+ channel blockers and the cholinergic agonists were infused and injected, respectively, into the adrenal gland. The voltage-dependent K+ 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 Ca2+-activated K+ (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.

adrenal gland; mast cell degranulating peptide; scyllatoxin; voltage-dependent potassium channels; small-conductance calcium-activated potassium channels


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