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


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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    ABSTRACT: In their native environment, gulf toadfish excrete equal quantities of ammonia and urea. However, upon exposure to stressful conditions in the laboratory (i.e. crowding, confinement or air exposure), toadfish decrease branchial ammonia excretion and become ureotelic. The objective of this study was to determine the influences of cortisol and ammonia on ammonia excretion relative to expression of Rhesus (Rh) glycoproteins and the ammonia-fixing enzyme, glutamine synthetase (GS). In vivo infusions and/or injections were used to manipulate corticosteroid activity and plasma ammonia concentrations in ureotelic toadfish. Metyrapone treatment to lower circulating cortisol levels resulted in a 3.5-fold elevation of ammonia excretion rates, enhanced mRNA expression of two of the toadfish Rh isoforms (Rhcg1 and Rhcg2), and decreased branchial and hepatic GS activity. Correspondingly, cortisol infusion decreased ammonia excretion 2.5-fold, a change that was accompanied by reduced branchial expression of all toadfish Rh isoforms (Rhag, Rhbg, Rhcg1 and Rhcg2) and a twofold increase in hepatic GS activity. In contrast, maintenance of high circulating ammonia levels by ammonia infusion enhanced ammonia excretion and Rh expression (Rhag, Rhbg and Rhcg2). Toadfish treated with cortisol showed an attenuated response to ammonia infusion with no change in Rh mRNA expression or GS activity. In summary, the evidence suggests that ammonia excretion in toadfish is modulated by cortisol-induced changes in both Rh glycoprotein expression and GS activity.
    Full-text · Article · Jan 2012 · Journal of Experimental Biology
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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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    ABSTRACT: Cooperation often involves a conflict of interest. This is particularly true in situations where one individual seeks out a service but cannot properly control the quality of the service given by the partner who would gain from defecting. An example is cleaning mutualism involving the bluestreak cleaner wrasse (Labroides dimidiatus) and its reef-fish 'clients'. These cleaners may reduce the stress experienced by their clients by removing parasites; however they occasionally cheat clients (i.e. defect) by eating mucus and other living tissues. Here we present experimental support for the hypothesis that stress responses increase the motivation for clients to seek out such risky asymmetric interactions. We manipulated the stress response by blocking glucocorticoid receptors with the antagonist RU486 in a species that is a regular visitor of cleaner fish, the lined bristletooth (Ctenochaetus striatus). Field observations 1 week after treatment with RU486 showed that antagonist treatment led to a reduction in cleaning duration compared to control treatment. This was not explained by a general effect on client behavior as intraspecific social behavior appeared unaffected. We propose that antagonist treatment reduced stress responses to the presence of ectoparasites, which in turn reduced the client's perception of benefits from seeking out cleaning interactions. The results demonstrate a hitherto overlooked variable role of stress and stress responses on cooperative behavior.
    Full-text · Article · Jan 2012 · Hormones and Behavior
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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.
    Full-text · Article · Jun 2009 · Journal of Experimental Biology
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