Abstract
Acetylcholine (ACh, 100 μM)-evoked catecholamine release from perfused bovine adrenal glands was unaffected by CTX (0.3 μM) and depressed 70% by nisoldipine (1 μM). Combined CTX plus nisoldipine did not inhibit further the secretory response. K+ (150 mM)-evoked secretion was diminished 30% by CTX and 20% by nisoldipine. Combined CTX plus nisoldipine inhibited secretion by 35%. Cd2+ blocked the K+-evoked secretory response by over 90%. Bay K 8644 (1 μM) enhanced the basal output of catecholamines and clearly potentiated the secretory responses to mild concentrations of ACh (3 μM) or K+ (17.7 mM). The results suggest that in addition to CTX- and DHP-sensitive Ca2+ channels, a third Ca2+ pathway might contribute to the entry of external Ca2+ into chromaffin cells necessary to trigger the exocytotic catecholamine release response in the bovine adrenal gland.
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