Abstract

Histological observations have confirned the existence of more or less linked relationships between the pituitary and interrenals in the teleosts, as in mammals. More recently, variations of the glandular activity of the pituitary-interrenal system in relation to external salinity changes have revealed that its secretion is involved in the control of osmoregulation of euryhaline teleosteans. Various experimental procedures, especially pharmacological or surgical ablation of the endocrine glands, produce overall changes in water and electrolyte composition of the extra- and intracellular fluids of the eel or other teleosts. Isotopic kinetic techniques have permitted the study of the mechanisms of ionic transfer and their endocrine control, and have shown that—besides the kidney—the gills and the gut are target organs of the adrenosteroids. Most of the studies have been done on Anguilla anguilla, Fundulus heteroclitus, and F. kansae. In the seawater animals, a rapid turnover involving about 30–50% of the exchangeable internal sodium per hour is observed. The net excretion of salt through the gill represents about one-tenth to one-fifth of the total outflux, the renal sodium loss being negligible. Salt absorption through the gut accompanying drinking and water uptake corresponds to a similar fraction of the total influx. Hypophysectomy is followed by a significant reduction of the sodium exchange, a diminution of the salt excretion through the gills, and a reduction of salt and water absorption through the gut. Injections of ACTH and cortisol are able to restore normal gill sodium turnover rates and gut function. Adrenalectomy is followed by an even bigger diminution of the gill sodium exchange and salt excretion. Injections of small doses of cortisol are able to bring back normal sodium exchange and normal electrolyte plasma level. In intact eels, ACTH and cortisol as well as aldosterone injections produce an augmentation of the sodium turnover rate above the normal level. Interrenalectomized eels survive poorly in seawater and better in freshwater; when transferred back to seawater, the gill outflux adaptation pattern is considerably slowed down. In the freshwater-adapted animals, a slow sodium turnover is observed, involving 0.5% of the internal sodium per hour at most. The renal sodium loss is compensated by the gill net sodium intake, which represents about one-third to one-half of the gill influx. Hypophysectomy produces a diminution of the net sodium uptake, but it is the absence of prolactin-like factor which is responsible for this defect, due to an augmentation of the gill outflux. Adrenalectomy is followed by a reduction of the sodium influx. Injections of aldosterone or cortisol at low doses produce an increase of the sodium net uptake, as a result of an enhancement of the sodium influx. Higher doses of cortisol induce sodium loss through the gills. The cellular mechanism of adrenosteroid action in the gills is discussed in the light of recent observations obtained in other groups of vertebrates. In any case, cortisol is to be considered as a mineralocorticoid in teleosts. It plays the role of a salt-excreting factor in the fish living in hypertonic media, and as a salt absorbing factor in the freshwater-adapted teleosteans.

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