In:
American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, American Physiological Society, Vol. 279, No. 2 ( 2000-08-01), p. R448-R454
Abstract:
We elucidated the functional contribution of K + channels to cholinergic control of catecholamine secretion in the perfused rat adrenal gland. The small-conductance Ca 2+ -activated K + (SK Ca )-channel blocker apamin (10–100 nM) enhanced the transmural electrical stimulation (ES; 1–10 Hz)- and 1,1-dimethyl-4-phenyl-piperazinium (DMPP; 5–40 μM)-induced increases in norepinephrine (NE) output, whereas it did not affect the epinephrine (Epi) responses. Apamin enhanced the catecholamine responses induced by acetylcholine (6–200 μM) and methacholine (10–300 μM). The putative large-conductance Ca 2+ -activated K + channel blocker charybdotoxin (10–100 nM) enhanced the catecholamine responses induced by ES, but not the responses induced by cholinergic agonists. Neither the K A channel blocker mast cell degranulating peptide (100–1000 nM) nor the K V channel blocker margatoxin (10–100 nM) affected the catecholamine responses. These results suggest that SK Ca channels play an inhibitory role in adrenal catecholamine secretion mediated by muscarinic receptors and also in the nicotinic receptor-mediated secretion of NE, but not of Epi. Charybdotoxin-sensitive Ca 2+ -activated K + channels may control the secretion at the presynaptic site.
Type of Medium:
Online Resource
ISSN:
0363-6119
,
1522-1490
DOI:
10.1152/ajpregu.2000.279.2.R448
Language:
English
Publisher:
American Physiological Society
Publication Date:
2000
detail.hit.zdb_id:
1477297-8
SSG:
12
