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Biomedical subjects

M Danielle McDonald

Publications and source records attributed to M Danielle McDonald.

14 recordsLinked to original sources
PubMed2006

Is urea pulsing in toadfish related to environmental O2 or CO2 levels?

The neurochemical, serotonin (5-hydroxytryptamine; 5-HT) is involved in the regulation of toadfish pulsatile urea excretion as well as the teleost hypoxia response. Thus, the goal of this study was to determine whether environmental conditions that activate branchial chemoreceptors also trigger pulsatile urea excretion in toadfish, since environmental dissolved oxygen levels in a typical toadfish habitat show significant diel fluctuations, often reaching hypoxic conditions at dawn. Toadfish were fitted with arterial, venous and/or buccal catheters and were exposed to various environmental conditions, and/or injected with the O(2) chemoreceptor agonist NaCN or the 5-HT(2) receptor agonist alpha-methyl-5HT. Arterial PO(2), as well as ammonia and urea excretion were monitored. Natural fluctuations in arterial PO(2) levels in toadfish did not correlate with the occurrence of a urea pulse. Chronic exposure (24 h) of toadfish to hyperoxia was without effect on nitrogen excretion, however, exposure to hypoxia caused a significant reduction in the frequency of urea pulses, and exposure to hypercapnia resulted in a reduction in the percentage of nitrogen waste excreted as urea. Of toadfish exposed acutely to hypoxia, 20% pulsed within 1 h, whereas none pulsed after normoxic or hypercapnic treatments. Furthermore, 20% of fish injected intravenously with NaCN pulsed within 1 h of injection, but no fish pulsed after injection of NaCN into the buccal cavity. To test whether environmental conditions affected 5-HT(2) receptors, toadfish were injected with alpha-methyl-5HT, which elicits urea pulses in toadfish. No significant differences in pulse size occurred among the various environmental treatments. Our findings suggest that neither the environmental conditions of hypoxia, hyperoxia or hypercapnia, nor direct branchial chemoreceptor activation by NaCN play a major role in the regulation of pulsatile urea excretion in toadfish.

Animals↗
PubMed2006

Piscine insights into comparisons of anoxia tolerance, ammonia toxicity, stroke and hepatic encephalopathy.

Although the number of fish species that have been studied for both hypoxia/anoxia tolerance and ammonia tolerance are few, there appears to be a correlation between the ability to survive these two insults. After establishing this correlation with examples from the literature, and after examining the role Peter Lutz played in catalyzing this convergent interest in two variables, this article explores potential mechanisms underpinning this correlation. We draw especially on the larger body of information for two human diseases with the same effected organ (brain), namely stroke and hepatic encephalopathy. While several dissimilarities exist between the responses of vertebrates to anoxia and hyperammonemia, one consistent observation in both conditions is an overactivation of NMDA receptors or glutamate neurotoxicity. We propose a glutamate excitotoxicity hypothesis to explain the correlation between ammonia and hypoxia resistance in fish. Furthermore, we suggest several experimental paths to test this hypothesis.

Adaptation, Physiological↗
PubMed2006

Hydromineral balance in the marine gulf toadfish (Opsanus beta) exposed to waterborne or infused nickel.

The effects of acute Ni exposure on the marine gulf toadfish (Opsanus beta) were investigated via separate exposures to waterborne nickel (Ni) and arterially infused Ni. Of the plasma electrolytes measured after 72 h of waterborne exposure (215.3 and 606.1 microM Ni in SW (salinity of 34)), only plasma [Ca2+] was significantly impacted (approximately 55% decrease at both exposure concentrations). At both exposure concentrations, plasma [Ni] was regulated for 24h, after which a linear accumulation over time occurred. Accumulation of Ni in the plasma, and in tissues in direct contact with seawater (gill, stomach, and intestine), was roughly proportional to the Ni concentration of the exposure water. Hydromineral balance in the intestinal fluid (IF) was markedly impacted, with Na(+), Cl(-), SO(4)(2-), K+, and Mg2+ concentrations elevated after 72 h of exposure to waterborne Ni. Following arterial Ni infusion (0.40 micromolNikg(-1)h(-1)), perturbation of hydromineral balance of the intestinal fluid was specific only to Na+ (significantly elevated by Ni infusion) and Mg2+ (significantly decreased by Ni infusion). Nitrogen excretion was not significantly impacted by Ni infusion. In all tissues save the kidney, Ni accumulation via infusion was only a fraction of that observed during waterborne exposures. Remarkably, the kidney Ni burden following infusion was almost identical to that resulting from both waterborne exposures, suggesting homeostatic control. Ni excretion, dominated at 24 h by extrarenal routes, was primarily a function of renal excretion by 72 h of infusion. The sum excretion from infused toadfish was relatively efficient, accounting for over 40% of the infused dose by 72 h. Mechanistic knowledge of the mechanisms of toxicity of waterborne Ni in marine systems is a critical component to the development of physiologically based modeling approaches to accurately predict Ni toxicity in marine and estuarine ecosystems.

Animals↗
PubMed2006

Maintaining osmotic balance with an aglomerular kidney.

The gulf toadfish, Opsanus beta, is a marine teleost fish with an aglomerular kidney that is highly specialized to conserve water. Despite this adaptation, toadfish have the ability to survive when in dilute hypoosmotic seawater environments. The objectives of this study were to determine the joint role of the kidney and intestine in maintaining osmotic and ionic balance and to investigate whether toadfish take advantage of their urea production ability and use urea as an osmolyte. Toadfish were gradually acclimated to different salinities (0.5, 2.5, 5, 10, 15, 22, 33, 50 and 70 ppt (1.5%, 7.5%, 15%, 30%, 45%, 67%, 100%, 151% and 212% seawater)) and muscle tissue, urine, blood and intestinal fluids were analyzed for ion and in some cases urea concentration. The renal and intestinal ionoregulatory processes of toadfish responded to changes in salinity and when gradually acclimated, toadfish maintain a relatively constant plasma osmolality at environmental salinities of 5 to 50 ppt. However, at salinities lower (2.5 ppt) or higher (70 ppt) than this range, a significant deviation from resting plasma and urine osmolality as well as changes in muscle water content was measured, suggesting osmoregulatory difficulties at these salinities. The renal system compensates for dilute seawater by reducing Na+ reabsorption by the bladder, which allowed excess water to be excreted. In the case of hypersalinity, Na+ reabsorption was increased, which resulted in a conservation of water and the concentration of Mg2+, Cl-, SO(4)2- and urea. A similar pattern was observed within the gastrointestinal system. Notably, Mg2+, HCO3- and SO4(2-) were the dominant ions in the intestinal fluid under control and hypersaline conditions due to the absorption of Na+, Cl- and water. When exposed to dilute seawater conditions, the absorption of Na+ was greatly reduced which likely increased water elimination. As a result of decreased environmental levels and a reduction in drinking rate, Mg2+ and SO4(2-) in intestinal fluids under hypoosmotic conditions were greatly reduced. While urea did play a minor role in renal osmoregulation, toadfish appear to preferentially regulate Na+ and to some extend Cl- in urine and intestinal fluids.

Acclimatization↗
PubMed2005

Ammonia affects brain nitrogen metabolism but not hydration status in the Gulf toadfish (Opsanus beta).

Laboratory rodents made hyperammonemic by infusing ammonia into the blood show symptoms of brain cell swelling and increased intracranial pressure. These symptoms could be caused in part by an increase in brain glutamine formed when brain glutamine synthetase (GS) naturally detoxifies ammonia to glutamine. Previous studies on the Gulf toadfish (Opsanus beta) demonstrated that it is resistant to high ammonia exposure (HAE) (96 h LC(50)=10mM) despite an increase in brain glutamine. This study attempts to resolve whether the resistance of O. beta is mediated by special handling of brain water in the face of changing glutamine concentrations. Methionine sulfoximine (MSO), an inhibitor of GS, was used to pharmacologically manipulate glutamine concentrations, and magnetic resonance imaging (MRI) was used to assess the status of brain water. Ammonia or MSO treatment did not substantially affect blood acid-base parameters. Exposure to 3.5mM ammonium chloride in seawater for 16 or 40 h resulted in a parallel increase in brain ammonia (3-fold) and glutamine (2-fold) and a decrease in brain glutamate (1.3-fold). Pre-treatment with MSO prevented ammonia-induced changes in glutamine and glutamate concentrations. HAE also induced an increase in plasma osmolality (by 7%) which was probably due to a disturbance of osmoregulatory processes but which did not result in broader whole body dehydration as indicated by muscle water analysis. The increase in brain glutamine was not associated with any changes in brain water in toadfish exposed to 3.5 mM ammonia for up to 40 h or even at 10, 20 and 30 mM ammonia consecutively and for one hour in each concentration. The lack of brain water accumulation implies that ammonia toxicity in toadfish appears to be via pathways other than cerebral swelling. Furthermore, toadfish pre-treated with MSO did not survive a normally sub-lethal exposure to 3.5 mM ammonia for 40 h. The enhancement of ammonia toxicity by MSO suggests that GS function is critical to ammonia tolerance in this species.

Ammonia↗
PubMed2005

Does pulsatile urea excretion serve as a social signal in the gulf toadfish Opsanus beta?

This study evaluated the hypothesis that the pulsatile excretion of urea by toadfish could serve as a social signal. In the first experiment, physiological parameters were measured in pairs of dominant and subordinate toadfish. Subordinate toadfish had elevated concentrations of circulating plasma cortisol, an effect maintained even after cannulation. In the second experiment, one fish of a pair was injected with 14C-urea, and the occurrence of urea pulses during social encounters was documented. Social status did not influence the order of pulsing, that is, whether a dominant or subordinate fish pulsed first during a social encounter. However, in seven out of eight pairs, both toadfish pulsed within 2 h of each other, indicating some form of communication between fish. In the third and final experiment, the response of toadfish to urea (natural or synthetic) was observed. There was a tendency for toadfish to avoid synthetic urea but there was no apparent behavioural response to water containing toadfish urea. Pulsing events do not appear to play an integral role during social encounters as previously hypothesised, but the close timing of pulses in toadfish pairs suggests some transfer of information.

Aggression↗
PubMed2004

Bioavailability of silver and its relationship to ionoregulation and silver speciation across a range of salinities in the gulf toadfish (Opsanus beta).

Silver is taken up as a Na(+) analog (Ag(+)) by freshwater organisms, but little is known about its bioavailability in relation to salinity. Adult Opsanus beta were acclimated to 2.5, 5, 10, 20, 40, 60, 80, and 100% seawater (Cl(-)=545 mM) and exposed for 24 h to 2.18 microg L(-1) silver as (110m)Ag-labelled AgNO(3), a concentration close to the U.S. EPA marine criterion and less than 0.1% of the acute 96-h LC50 in seawater. Plasma osmolality, Na(+), and Cl(-) remained approximately constant from 100% down to 20-40% seawater, thereafter declining to 89% (osmolality) and 82% (Na(+), Cl(-)) of seawater values at the lowest salinity (2.5% seawater), while plasma Mg(2+) was invariant. Ionic measurements in intestinal fluids and urine supported the view that above the isosmotic point (about 32% seawater), toadfish drink the medium, absorb Na(+), Cl(-), and water across the gastrointestinal tract, actively excrete Na(+) and Cl(-) across the gills, and secrete Mg(2+) into the urine. Below this point, toadfish appear to stop drinking, actively take up Na(+) and Cl(-) at the gills, and retain ions at the kidney. Silver accumulation varied greatly with salinity, by nine-fold (whole body), 26-fold (gill tissue), and 18-fold (liver), with the maxima occurring in 2.5% seawater, the minima in 40% seawater (close to the isosmotic point), and slightly greater values at higher salinities. Highest silver concentrations occurred in liver, second highest in gills, intermediate concentrations in kidney, spleen, and gastrointestinal tissues, and lowest in swim bladder and white muscle, though patterns changed with salinity. There were substantial biliary but minimal urinary levels of silver. The salinity-dependent pattern of silver accumulation best correlated with the abundance of the neutral complex AgCl(0), though the presence of small amounts of Ag(+) at the lowest salinities may also have been important. In contrast, silver accumulation in the esophagus-stomach was greatest in 100% seawater and least at the isosmotic salinity (five-fold variation), a pattern probably explained by drinking and silver uptake into the blood through the gills. Models of silver bioavailability across salinity must consider the presence of silver-binding ligands on both gills and gastrointestinal tract, changing silver speciation, and the changing ionoregulatory physiology of the organism.

Animals↗
PubMed2004

Evidence for facilitated diffusion of urea across the gill basolateral membrane of the rainbow trout (Oncorhynchus mykiss).

Recent in vivo evidence suggests that the mechanism of branchial urea excretion in the ammoniotelic rainbow trout (Oncorhynchus mykiss) is carrier-mediated. Further characterization of this proposed mechanism was achieved by using an in vitro isolated basolateral membrane vesicle (BLMV) preparation in which isolated gill membranes were used to determine a variety of physiological properties of the transporter. BLMV demonstrated two components of urea uptake, a linear component at concentrations up to 17.5 mmol x l(-1) and a saturable component (K(0.5)=0.35+/-0.01 mmol x l(-1); V(max)=0.14+/-0.02 micromol mg protein(-1) h(-1)) with a Hill constant of 1.35+/-0.18 at low, physiologically relevant urea concentrations (<2 mmol x l(-1)). Saturable uptake of urea at 1 mmol x l(-1) by BLMV was reduced by 88.5% when incubated with 0.25 mmol x l(-1) phloretin, a potent blocker of UT-type facilitated diffusion urea transport mechanisms. BLMV also demonstrated differential handling of urea versus urea analogues at 1 mmol x l(-1) concentrations and total analogue/total urea uptake ratios were 32% for acetamide and 84% for thiourea. Saturable urea uptake at 1 mmol x l(-1) was significantly reduced by almost 100% in the presence of 5 mmol x l(-1) thiourea but was not affected by 5 mmol x l(-1) acetamide or 5 mmol x l(-1) N-methylurea. Lastly, total urea uptake at 1 mmol x l(-1) by BLMV was sensitive to temperatures above and below the temperature of acclimation with a Q(10)>2 suggesting a protein carrier-mediated process. Combined, this evidence indicates that a facilitated diffusion urea transport mechanism is likely present in the basolateral membrane of the rainbow trout gill.

Acclimatization↗
PubMed2004

Dogmas and controversies in the handling of nitrogenous wastes: 5-HT2-like receptors are involved in triggering pulsatile urea excretion in the gulf toadfish, Opsanus beta.

When injected arterially, serotonin (5-hydroxytryptamine; 5-HT) has been shown to elicit naturally sized urea pulse events in the gulf toadfish, Opsanus beta. The goal of the present study was to determine which 5-HT receptor(s) was involved in mediating this serotonergic stimulation of the pulsatile excretion mechanism. Toadfish were surgically implanted with caudal arterial catheters and intraperitoneal catheters and injected with either 8-OH-DPAT (1 micro mol kg(-1)), a selective 5-HT(1A) receptor agonist, alpha-methyl-5-HT (1 micro mol kg(-1)), a 5-HT(2) receptor agonist, or ketanserin, a 5-HT(2) receptor antagonist (0.01, 0.1, 1 and 10 micro mol kg(-1)) plus alpha-methyl-5-HT. 8-OH-DPAT injection did not mediate an increase in urea excretion, ruling out the involvement of 5-HT(1A) receptors in pulsatile excretion. However, within 5 min, alpha-methyl-5-HT injection caused an increase in the excretion of urea in >95% (N=27) of the fish injected, with an average pulse size of 652+/-102 micro mol N kg(-1) (N=26). With alpha-methyl-5-HT injection there was no corresponding increase in ammonia or [(3)H]PEG 4000 permeability. Urea pulses elicited by alpha-methyl-5-HT were inhibited in a dose-dependent fashion by the 5-HT(2) receptor antagonist ketanserin, which at low doses caused a significant inhibition of pulse size and at higher doses significantly inhibited the occurrence of pulsatile excretion altogether. However, neither 8-OH-DPAT nor alpha-methyl 5-HT injection had an effect on plasma cortisol or plasma urea concentrations. These findings suggest the involvement of a 5-HT(2)-like receptor in the regulation of pulsatile urea excretion.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed2003

Branchial and renal handling of urea in the gulf toadfish, Opsanus beta: the effect of exogenous urea loading.

The objective of this study was to determine whether the pulsatile facilitated diffusion transport mechanism (tUT) found in the gills of the gulf toadfish (Opsanus beta) and the active secretion transporter thought to be present in its kidney could be saturated when faced with elevated plasma urea concentrations. Toadfish were infused with four consecutive exogenous urea loads at a rate of 0, 150, 300 and 600 micromol kg(-1) h(-1). Initial plasma and urine urea concentrations were 8.1+/-0.9 and 12.4+/-1.5 mmol l(-1), respectively, and steadily increased with increasing infused loads of urea to a maximum of 36.8+/-2.8 mmol l(-1) in the plasma and 39.8+/-6.5 mmol l(-1) in the urine. There was only a very weak relationship (r=0.17) between pulse size (measured as branchial excretion during pulsatile excretion of urea) and plasma urea concentration (slope=9.79 micromol-N kg(-1) per mmol-N l(-1); P<0.05) suggesting that the branchial excretion mechanism was already saturated at normal plasma urea concentrations. Urine flow rate (0.15+/-0.03 ml kg(-1) h(-1)) and glomerular filtration rate (0.025+/-0.004 ml kg(-1) h(-1)) remained constant throughout the experiment despite the increased volume load. Renal urea secretion rate maintained a strong linear relationship (r=0.84) to plasma urea levels (slope=0.391 micromol-N kg(-1) h(-1) per mmol-N l(-1); P<0.001) with no observable transport maximum, suggesting that the renal secretory transport mechanism was not saturated even at plasma urea levels well above normal, in contrast to the branchial excretion mechanism.

Animals↗
PubMed2003

Pulsatile urea excretion in the gulf toadfish: mechanisms and controls.

Opsanus beta expresses a full complement of ornithine-urea cycle (OUC) enzymes and is facultatively ureotelic, reducing ammonia-N excretion and maintaining urea-N excretion under conditions of crowding/confinement. The switch to ureotelism is keyed by a modest rise in cortisol associated with a substantial increase in cytosolic glutamine synthetase for trapping of ammonia-N and an upregulation of the capacity of the mitochondrial OUC to use glutamine-N. The entire day's urea-N production is excreted in 1 or 2 short-lasting pulses, which occur exclusively through the gills. The pulse event is not triggered by an internal urea-N threshold, is not due to pulsatile urea-N production, but reflects pulsatile activation of a specific branchial excretion mechanism that rapidly clears urea-N from the body fluids. A bidirectional facilitated diffusion transporter, with pharmacological similarity to the UT-A type transporters of the mammalian kidney, is activated in the gills, associated with an increased trafficking of dense-cored vesicles in the pavement cells. An 1814 kB cDNA ('tUT') coding for a 475-amino acid protein with approximately 62% homology to mammalian UT-A's has been cloned and facilitates phloretin-sensitive urea transport when expressed in Xenopus oocytes. tUT occurs only in gill tissue, but tUT mRNA levels do not change over the pulse cycle, suggesting that tUT regulation occurs at a level beyond mRNA. Circulating cortisol levels consistently decline prior to a pulse event and rise thereafter. When cortisol is experimentally clamped at high levels, natural pulse events are suppressed in size but not in frequency, an effect mediated through glucocorticoid receptors. The cortisol decline appears to be permissive, rather than the actual trigger of the pulse event. Fluctuations in circulating AVT levels do not correlate with pulses; and injections of AVT (at supraphysiological levels) elicit only minute urea-N pulses. However, circulating 5-hydroxytryptamine (5-HT) levels fluctuate considerably and physiological doses of 5-HT cause large urea-N pulse events. When the efferent cranial nerves to the gills are sectioned, natural urea pulse events persist, suggesting that direct motor output from the CNS to the gill is not the proximate control.

Adaptation, Physiological↗
PubMed2002

Transport physiology of the urinary bladder in teleosts: a suitable model for renal urea handling?

The transport physiology of the urinary bladder of both the freshwater rainbow trout (Oncorhychus mykiss) and the marine gulf toadfish (Opsanus beta) was characterized with respect to urea, and the suitability of the urinary bladder as a model for renal urea handling was investigated. Through the use of the in vitro urinary bladder sac preparation urea handling was characterized under control conditions and in the presence of pharmacological agents traditionally used to characterize urea transport such as urea analogues (thiourea, acetamide), urea transport blockers (phloretin, amiloride), and hormonal stimulation (arginine vasotocin; AVT). Na(+)-dependence and temperature sensitivity were also investigated. Under control conditions, the in vitro trout bladder behaved as in vivo, demonstrating significant net reabsorption of Na(+), Cl(-), water, glucose, and urea. Bladder urea reabsorption was not affected by pharmacological agents and, in contrast to renal urea reabsorption, was not correlated to Na(+). However, the trout bladder showed a threefold greater urea permeability compared to artificial lipid bilayers, a prolonged phase transition with a lowered E(a) between 5 degrees C and 14 degrees C, and differential handling of urea and analogues, all suggesting the presence of a urea transport mechanism. The in vitro toadfish bladder did not behave as in vivo, showing significant net reabsorption of Na(+) but not of Cl(-), urea, or water. As in the trout bladder, pharmacological agents were ineffective. The toadfish bladder showed no differential transport of urea and analogues, consistent with a low permeability storage organ and intermittent urination. Our results, therefore, suggest the possibility of a urea transport mechanism in the urinary bladder of the rainbow trout but not the gulf toadfish. While the bladders may not be suitable models for renal urea handling, the habit of intermittent urination by ureotelic tetrapods and toadfish seems to have selected for a low permeability storage function in the urinary bladder.

Animals↗
PubMedDate not supplied

Differential handling of urea and its analogues suggests carrier-mediated urea excretion in freshwater rainbow trout.

The possible presence of urea transport mechanisms in the gill and kidney of the freshwater rainbow trout (Oncorhynchus mykiss) was investigated in vivo by comparing the branchial and renal handling of analogues acetamide and thiourea with the handling of urea. Trout were fitted with indwelling dorsal aortic catheters and urinary catheters and injected with an isosmotic dose of [(14)C]-labeled urea analogue (acetamide or thiourea) calculated to bring plasma analogue concentrations close to plasma urea concentrations. Urea and analogue concentrations were significantly greater in the urine than in the plasma. Branchial clearance rate of acetamide was only 48% of urea clearance, whereas the clearance of thiourea was only 22%, a pattern that was also observed in branchial uptake of these substances and was similar to our previous observations in toadfish and midshipmen. The renal secretion clearance rates of urea and acetamide were similar, and on average, both substances were secreted on a net basis, although reabsorption did occur in some cases. In contrast, thiourea was neither reabsorbed nor secreted by the kidney tubule. The secretion clearance rates of both acetamide and urea were well correlated with the secretion clearance rates of Na(+), Cl(-), and water, whereas there was no relationship between thiourea and these substances. The pattern of acetamide, thiourea, and urea handling by the gill of the trout is similar to that found in the gills of the midshipman and the gulf toadfish and strongly suggests the presence of a UT-type facilitated diffusion urea transport mechanism. The pattern of differential handling in the kidney is unlike that in the gill and also unlike that in the kidney of the midshipman and the gulf toadfish, suggesting a different mechanism. In addition, renal urea secretion occurs against a concentration gradient, suggesting the involvement of an active transport mechanism.

Acetamides↗