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The effect of ovine GH (oGH) in vivo and recombinant bovine insulin-like growth factor-I (rbIGF-I) in vitro on gill Na+,K+-ATPase activity was investigated in two seasonal experiments conducted during the parr–smolt transformation period of coho salmon.
In 1991, when fish were held under a photoperiod of 12 h light: 12 h darkness, the stimulatory effect of oGH (1 µg/g) on gill Na+,K+-ATPase in vivo decreased at the time of expected parr–smolt transformation. Gill Na+,K+-ATPase from control fish was insensitive to rbIGF-I in vitro from February to June, whereas GH treatment induced sensitivity to rbIGF-I (100–1000 µg/l) in vitro in February and March, but not later in development.
In 1992, when fish were held under natural conditions, oGH (4 µg/g) stimulated gill Na+,K+-ATPase in vivo from February to July. There was, however, a pronounced developmental change in sensitivity of gill Na+,K+-ATPase to rbIGF-I in vitro. In February, gills from control fish were insensitive, but oGH treatment in vivo induced sensitivity to rbIGF-I in vitro (100–1000 µg/l). In April and May, control fish were sensitive to rbIGF-I in vitro. This sensitivity was not further potentiated by oGH treatment in vivo. In June, gills from control or oGH-treated fish were not sensitive to rbIGF-I in vitro, but in July exogenous oGH again induced gill tissue sensitivity to rbIGF-I at 1000 µg/l. Both studies showed that rbIGF-I stimulates gill Na+,K+-ATPase directly; an ability that may depend on priming by endogenous or exogenous GH. This supports the role of IGF-I as an endocrine mediator for GH action during parr–smolt transformation.
Journal of Endocrinology (1993) 138, 23–30
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