Article

Glucocorticoid receptors are involved in the regulation of pulsatile urea excretion in toadfish

Department of Biology, McMaster University, Hamilton, Ontario L8S 4K1, Canada.
Journal of Comparative Physiology B (Impact Factor: 2.62). 12/2004; 174(8):649-58. DOI: 10.1007/s00360-004-0456-y
Source: PubMed

ABSTRACT

The objectives of this study were to characterize the pattern of pulsatile urea excretion in the gulf toadfish in the wake of exogenous cortisol loading and to determine the receptors involved in the regulation of this mechanism. Toadfish were fitted with indwelling arterial catheters and were infused with isosmotic NaCl for 48 h after which fish were treated with cortisol alone, cortisol + peanut oil, cortisol + RU486 (a glucocorticoid receptor antagonist) or cortisol + spironolactone (a mineralocorticoid receptor antagonist). Upon cortisol loading, fish treated with cortisol alone, cortisol + oil or cortisol + spironolactone experienced a two- to threefold reduction in pulsatile urea excretion. This reduction was due to a decrease in urea pulse size with no effect on pulse frequency compared to values measured during the control NaCl infusion period. In addition, these fish showed an increase in plasma urea concentrations upon treatment. These apparent effects of cortisol treatment were abolished in fish treated with cortisol + RU486. In contrast, these fish showed an increase in pulsatile urea excretion mediated by a twofold increase in pulse size with no change in frequency. Likewise, fish treated with cortisol + RU486 showed a significant decrease in plasma urea concentrations over the course of the experiment. The findings of this study indicate that high levels of cortisol reduce pulsatile urea excretion by decreasing pulse size. In addition, it appears that glucocorticoid receptors and not mineralocorticoid receptors are involved in the regulation of the toadfish pulsatile urea excretion mechanism.

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Available from: M. Danielle Mcdonald
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    • "Following this period, fish were lightly anesthetized with MS-222 (1gl –1 buffered with 2gl –1 sodium bicarbonate, pH7.8), covered with moist towels and surgically implanted with caudal artery catheters (Wood et al., 1997; McDonald et al., 2000) and, in some cases, intraperitoneal catheters (see below) (McDonald and Walsh, 2004). Catheters were used to facilitate delivery of pharmacological agents and/or for blood sampling with minimal handling stress. "
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    • "We tested this hypothesis by measuring the effects of RU486 (Mifepristone) on cleaning visits. In teleosts RU486 has been regularly used as a glucocorticoid receptor antagonist (Bernier et al., 1999) and it has been shown to suppress cortisol mediated effects on a wide range of physiological traits (metabolism: Vijayan and Leatherland, 1992; Bernier and Peter, 2000; reproduction: Goos and Consten, 2002; osmotic stress: McDonald et al., 2004; Shaw et al., 2007), and behavioral traits (social status: DiBattista et al., 2005; vocalizations in fish: Remage-Healey and Bass, 2004; aggression: Schjolden et al., 2009). RU486 has also been shown to have high affinity to progesterone receptor complexes in mammals (Baulieu , 1991; Cadepond et al., 1997; Bury et al., 2003), and recently Chen et al. (2010) reported that RU486 blocked the effects of progesterone on androgen production in zebrafish testes. "
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    • "Normalized pulse size and frequency are expressed in relative units. In addition, urea or ammonia excretion values (μmol N kg –1 ) were calculated as described by McDonald et al. (McDonald et al., 2004) using the following equation: Excretion = (ΔC ϫ V f )/M , where ΔC is the increases in concentration (μmol l –1 ), V f was the volume of the experimental flux chambers (in liters) and the product of both variables was adjusted to the mass (M) of the individual fish (in kg). These values were used to calculate percentage ureotelism. "
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    ABSTRACT: Gulf toadfish, Opsanus beta, are one among a group of unusual teleosts that excrete urea as their predominant nitrogen end product in response to stressful conditions. Under conditions of crowding or confinement, fasted toadfish excrete the majority of their nitrogen waste in large pulses of urea (>90% of total nitrogen) lasting up to 3 h. An earlier study demonstrated that cortisol has an inhibitory influence on urea pulse size. The present study tested the hypothesis that cortisol mediates changes in urea pulse size in ureotelic toadfish through the glucocorticoid receptor (GR) and not the mineralocorticoid receptor (MR). In vivo pharmacological investigations were used to manipulate the corticosteroid system in crowded toadfish, including experimentally lowering plasma cortisol levels by the injection of metyrapone, blocking cortisol receptors through exposure to either RU-486 (GR antagonist) and spironolactone (MR antagonist), or through exogenous infusion of the tetrapod mineralocorticoid aldosterone (tetrapod MR agonist). The data demonstrate that lowering the activity of cortisol, either by inhibiting its synthesis or by blocking its receptor, resulted in a two- to threefold increase in pulse size with no accompanying change in pulse frequency. Treatment with spironolactone elicited a minor ( approximately 1.5-fold) reduction in pulse size, as did aldosterone treatment, suggesting that the anti-mineralocorticoid spironolactone has an agonistic effect in a piscine system. In summary, the evidence suggests that urea transport mechanisms in pulsing toadfish are upregulated in response to low cortisol, mediated primarily by GRs, and to a lesser extent MRs.
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