THE GILL CALCIUM-TRANSPORT CYCLE IN RAINBOW-TROUT IS CORRELATED WITH PLASMA-LEVELS OF BIOACTIVE, NOT IMMUNOREACTIVE, STANNIOCALCIN

Stanniocalcin (STC) is an inhibitor of gill Ca2+ transport that is pro duced by the corpuscles of Stannius, endocrine glands in bony fish. In young rainbow trout (Oncorhynchus mykiss), there are cyclical changes in the rate of gill Ca2+ transport, with alternating phases of accele rated and reduced uptake every 14 days. Previous studies by our labora tory have established that the responsiveness of young trout to the in hibitory effects of exogenous STC is dependent on this cycle. Trout ar e highly responsive to STC at peaks of Ca2+ uptake and unresponsive at nadirs, which has led us to suggest that the gill Ca2+ transport cycl e may be regulated by a reciprocal cycle in the levels of plasma STC. In this report, we have further characterized the gill Ca2+ transport cycle in salmonids and investigated the role of STC in its regulation. Our results showed that the cycle is synchronous and is likely a char acteristic feature in all salmonids but that it varies in amplitude be tween species. Surprisingly, we observed no correlation between circul ating levels of radioimmunoassayable STC and the rate of gill Ca2+ tra nsport in trout. To address this apparent contradiction, trout fry wer e passively immunized with STC antiserum to determine if there were va riable amounts of bioactive STC in the circulation, at times when trou t were either more or less sensitive to exogenous STC. We observed tha t during the times when trout were responsive to STC treatment (i.e., cycle peaks), passive immunization had no effect on the rate of gill C a2+ transport in fish from the same population, indicating that there were low levels of bioactive STC in the circulation. Conversely, durin g times when trout were insensitive to exogenous STC (i.e., cycle nadi rs), passive immunization significantly raised the rate of transport t hrough neutralization of endogenous STC, indicating that there were hi gh levels of bioactive hormone in the experimental population as a who le. The results suggest that the cycle is controlled by reciprocal cha nges in the amount of bioactive, but not immunoreactive, STC. As the t rout were capable of responding or were already responding to the effe cts of STC at all given times, this would rule out changes in the numb er of functional STC receptors as an explanation for these findings. A s a consequence, it appears that some factor is modifying the extent t o which circulating or secreted STC is biologically active and is ther efore exerting a higher level of control over gill Ca2+ transport.