Cano T M, Perry S F, Fenwick J C
Department of Biology, University of Ottawa, Ontario, Canada.
Gen Comp Endocrinol. 1994 Apr;94(1):1-10. doi: 10.1006/gcen.1994.1054.
An in vivo whole animal 45Ca influx bioassay was used to study the cholinergic control of the release of stanniocalcin (STC) in the rainbow trout (Oncorhynchus mykiss) and the American eel (Anguilla rostrata). In both species calcium influx (JinCa2+) was lowered in response to hypercalcemia induced by intravascular (trout) or intraperitoneal (eel) injections of CaCl2. In trout, this response was blocked by the cholinergic antagonist atropine (0.25 mumol kg-1) and mimicked by the cholinoceptor agonist carbachol (0.25 mumol kg-1). These observations are consistent with a cholinergic stimulation of STC release in response to hypercalcemia in trout. In eels, pretreatment with atropine did not block the lowering of JinCa2+ in response to hypercalcemia. This suggests that cholinergic stimulation is not obligatory for stanniocalcin release in eels. However, carbachol treatment did elicit STC release as revealed by the lowering of JinCa2+. This response to carbachol was not observed in stanniectomized eels. Thus, in the American eel it appears that there is a potential for cholinergic control of STC release but that other factors such as the local plasma calcium concentration may also be involved, at least in response to severe acute hypercalcemia.