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  • Author: D. J. Nichols x
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Male urine applied daily to their bedding raised the basal levels of plasma corticosterone in individually housed, virgin female mice, when compared with females (grouped or individually housed) living with male mice or with group-housed females exposed daily to male urine. Values were not affected during ether-induced stress. A single application of male urine raised plasma levels 30 min later regardless of housing conditions; but after 4 and 24 h levels had fallen to normal. The results are discussed in terms of sensitization of the pituitary-adrenal system and of stress and reproductive pheromones. Male urine was less effective than male presence at inducing 4-day oestrous cycles. Length and type of cycle varied continuously under the influence of a spectrum of environmental signals.

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D. J. Nichols, M. Weisbart and J. Quinn


Cortisol kinetics were examined in brook trout (Salvelinus fontinalis) to assess possible relationships with body fluid distribution during acclimation to sea water (SW). The disappearance curve of [3H]cortisol in plasma, after a bolus injection, was analysed by compartmental analysis using a three-pool mammillary model. The results indicated that only ∼ 10% of the total exchangeable cortisol was located in the plasma pool. Over 75% of the total cortisol was associated with a large slowly exchanging pool and the remaining cortisol was located in a second extravascular tissue pool which was in rapid exchange with the plasma pool.

Two days after transfer of trout from fresh water to SW, when plasma chloride concentration was at a new steady state, body weight, intracellular fluid volume, haematocrit and inulin clearance rate were lowered but plasma, blood and extracellular volumes were unaltered. Cortisol plasma clearance rate was unaltered but plasma cortisol concentration, cortisol secretion rate, total cortisol pool size and interpool transport rates were increased. These results are consistent with an acute role for cortisol in SW adaptation of brook trout.

The fraction of the total cortisol cleared was smaller and the average time that cortisol spent in the tissue pools was slightly longer in trout after transfer to SW, possibly reflecting altered fluid dynamics. The fractional disappearance rate was larger at higher plasma cortisol concentrations in the SW trout. This relationship is compatible with the hypothesis that cortisol protein binding protects cortisol from metabolism.

J. Endocr. (1985) 107, 57–69

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R. M. Shepherd, R. Fraser, D. J. Nichols and C. J. Kenyon


Angiotensin II (AII) stimulation of steroidogenesis is known to be associated with depolarization of the adrenocortical cell membrane. In these cells, membrane permeability to potassium ions governs electrical potential. The effects of All on the rate of efflux of K+ in relation to the control of aldosterone synthesis has been investigated in bovine adrenocortical cells preloaded with 43K.

In static incubations, the pattern of 43K efflux fitted a model with two exponential components with t ½ values of 47·7±1·7 and 14·2±0·6 (s.e.m.) min. AII increased the efflux rate of the slow-exchange component (t ½ 37·1±0·6 min) and retarded efflux from the fast-exchange component. With ouabain present to prevent reuptake of the isotope, the rate of efflux for both components was increased in unstimulated cells (t ½ 28·4±1·1 and 12·0±0·7 min). AII again increased the rate of efflux from the slow component (t ½ = 24·2±1·7 min, P < 0·01) and retarded efflux from the fast component. These biphasic effects were apparent in cells treated with a range of AII concentrations (0·1 nmol/l–1 μmol/l) but the point in time at which increased efflux from the slower component predominated over retardation of the slow component was earlier for cells treated with 1 μmol AII/l than for cells treated with lower concentrations.

We suggest that decreases and increases in K+ efflux caused by AII are associated with depolarization and repolarization respectively. Changes in intracellular concentrations of Ca2+ may link these events.

Journal of Endocrinology (1991) 128, 297–304