The Experts below are selected from a list of 153 Experts worldwide ranked by ideXlab platform
Richard D. Reina - One of the best experts on this subject based on the ideXlab platform.
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Salt Gland blood flow in the hatchling green turtle, Chelonia mydas.
Journal of comparative physiology. B Biochemical systemic and environmental physiology, 2000Co-Authors: Richard D. ReinaAbstract:Microsphere and morphometric techniques were used to investigate any circulatory changes that accompany secretion by the Salt Glands of hatchling Chelonia mydas. Salt Glands were activated by a Salt load of 27.0 mmol NaCl kg body mass (BM)−1, resulting in a mean sodium secretion rate of 4.14 ± 0.11 mmol Na kg BM−1 h−1 for a single Gland. Microsphere entrapment was approximately 160–180 times greater in the active Salt Gland than the inactive Gland, inferring a similar change in blood flow through Salt Gland capillaries. The concentration of microspheres trapped in the Salt Gland was significantly correlated with the rate of tear production (ml kg BM−1 h−1) and the total rate of sodium secretion (mmol Na kg BM−1 h−1) but not with tear sodium concentration (mmol Na l−1). Adrenaline (500 μg kg BM−1) inhibited tear production within 2 min and reduced microsphere entrapment by approximately 95% compared with active Glands. The volume of filled blood vessels increased from 0.03 ± 0.01% of secretory lobe volume in inactive Salt Gland sections to 0.70 ± 0.11% in active Gland sections. The results demonstrate that capillary blood flow in the Salt Gland of C. mydas can regulate the activity of the Gland as a whole.
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Control of Salt Gland activity in the hatchling green sea turtle, Chelonia mydas.
Journal of comparative physiology. B Biochemical systemic and environmental physiology, 2000Co-Authors: Richard D. Reina, Paul D. CooperAbstract:We studied the control of Salt Gland secretion in hatchling Chelonia mydas. The threshold Salt load to activate Salt secretion was between 400 μmol NaCl 100 g bodymass (BM)−1 and 600 μmol NaCl 100 g BM−1, which caused an increase in plasma sodium concentration of 13% to 19%. Following a Salt load of 2700 μmol NaCl 100 g BM−1, Salt Gland secretion commenced in 12 ± 1.3 min and reached maximal secretory concentration within 2–7 min. Maximal secretory rate of a single Gland averaged 415 μmol Na 100 g BM−1 h−1. Plasma sodium concentration and total osmotic concentration after Salt loading were significantly higher than pretreatment values within 2 min. Adrenalin (25 μg kg BM−1) and the cholinergic agonist methacholine (1 mg kg BM−1) inhibited Salt Gland activity. Atropine (10 mg kg BM−1) reversed methacholine inhibition and stimulated Salt Gland secretion when administered with a subthreshold Salt load. Arginine vasotocin produced a transient reduction in sodium secretion by the active Gland, while atrial natriuretic factor, vasoactive intestinal peptide and neuropeptide Y had no measurable effect on any aspect of Salt Gland secretion. Our results demonstrated that secretion of the Salt Gland in C. mydas can be modified by neural and hormonal chemicals in vivo and that the cholinergic and adrenergic stimulation of an exocrine Gland do not appear to have the typical, antagonist actions on the chelonian Salt Gland.
Maryanne R. Hughes - One of the best experts on this subject based on the ideXlab platform.
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Effect of melatonin on Salt Gland and kidney function of gulls, Larus glaucescens
General and comparative endocrinology, 2007Co-Authors: Maryanne R. Hughes, Nobu Kitamura, Darin C. Bennett, David A. Gray, Peter J. Sharp, Angela M.s. PoonAbstract:This study examined effects of exogenous melatonin on osmoregulatory hormones and water and sodium secretion by Salt Glands and excretion via the kidneys of Glaucous-winged gulls (Larus glaucescens). Six saline acclimated gulls were injected with inulin and paraminohippuric acid and then infused with 500 mM NaCl to stimulate Salt Gland secretion. Each bird was given infusions of NaCl alone and NaCl plus melatonin. Experiments were made one week apart in a randomized order. A large blood sample (to measure osmoregulatory hormones) was taken before infusion, at secretion, and at the end of infusion. A small blood sample was taken at the midpoint of each of six 10 min sequential collections of Salt Gland secretion and urine. Melatonin tended to increase plasma sodium concentration, did decrease plasma osmolality, but did not affect potassium concentration. Melatonin did not affect Salt Gland secretion rate or concentration nor renal plasma flow or glomerular filtration. Melatonin increased urine flow rate, tended to increase urine sodium concentration, and did decrease urine potassium concentration. Combined renal and extrarenal sodium excretion was greater during MT treatment. During NaCl infusion, angiotensin II increased, aldosterone decreased, and arginine vasotocin remained unchanged. Melatonin did not affect these responses. These data suggest an osmoregulatory role for melatonin in birds with Salt Glands.
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Effect of glucose on Salt Gland secretion in the glaucous-winged gull, Larus glaucescens.
Comparative Biochemistry and Physiology Part A: Physiology, 2005Co-Authors: Maryanne R. HughesAbstract:Abstract Intravenously or orally administered glucose had no effect on the concentration or volume of NaCl induced Salt Gland secretion in the gull, Larus glaucescens , although glucose is known to markedly increase the volume of secretion in the domestic duck.
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Comparison of renal and Salt Gland function in three species of wild ducks
Journal of Experimental Biology, 2003Co-Authors: Darin C. Bennett, Maryanne R. HughesAbstract:Three processes central to osmoregulation of marine birds were compared in three species of ducks that differ in habitat affinity, diet and saline tolerance. These processes are filtration of Na+ and water from the plasma by the kidneys, their reabsorption along the renal tubules, and secretion by the Salt Glands. Barrow's goldeneyes Bucephala islandica, the most marine species, have the highest rates for all three processes and only this species can secrete all the infused Salt via the Salt Glands. Rates of all three processes are lower in mallards Anas platyrhynchos, the most freshwater species. Following saline acclimation, mallards could excrete all the infused Na+ by a combined Na+ excretion of the kidneys and Salt Glands. Canvasbacks Aythya valisineria, despite being more saline tolerant than mallards, are unable to excrete all the infused Na+. They produce a large volume of urine (like mallards) that has a low [Na+] (like goldeneyes). Salt Gland secretion Na+ concentration did not differ among the three species, but only goldeneyes secrete at a rate sufficient to eliminate all infused Na+ via the Salt Glands. Differences in saline tolerance of these ducks species cannot be fully explained by differences in their filtration, reabsorption and secretion of Na+ and water, suggesting that the intestinal tract plays an important role.
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Regulation of Salt Gland, gut and kidney interactions.
Comparative biochemistry and physiology. Part A Molecular & integrative physiology, 2003Co-Authors: Maryanne R. HughesAbstract:Marine birds can drink seawater because their cephalic 'Salt' Glands secrete a sodium chloride (NaCl) solution more concentrated than seawater. Salt Gland secretion generates osmotically free water that sustains their other physiological processes. Acclimation to saline induces interstitial water and Na move into cells. When the bird drinks seawater, Na enters the plasma from the gut and plasma osmolality (Osm(pl)) increases. This induces water to move out cells expanding the extracellular fluid volume (ECFV). Both increases in Osm(pl) and ECFV stimulate Salt Gland secretion. The augmented intracellular fluid content should allow more rapid expansion of ECFV in response to elevated Osm(pl) and facilitate activation of Salt Gland secretion. To fully utilize the potential of the Salt Glands, intestinally absorbed NaCl must be reabsorbed by the kidneys. Thus, Na uptake at gut and renal levels may constrain extrarenal NaCl secretion. High NaCl intake elevates plasma aldosterone concentration of Pekin ducks and aldosterone stimulates intestinal and renal water and sodium uptake. High NaCl intake induces lengthening of the small intestine of adult Mallards, especially males. High NaCl intake has little effect on glomerular filtration rate or tubular sodium Na uptake of birds with competent Salt Glands. Relative to body mass, kidney mass and glomerular filtration rate (GFR) are greater in birds with Salt Glands than in birds that do not have them. Birds with Salt Glands do not change GFR, when they drink saline. Thus, their renal filtrate contains excess Na that is, in some species, almost completely renally reabsorbed and excreted in a more concentrated Salt Gland secretion. Na reabsorption by kidneys of other species, like mallards is less complete and their Salt Glands make less concentrated secretion. Such species may reflux urine into the hindgut, where additional Na may also be reabsorbed for extrarenal secretion. During exposure to saline, marine birds maintain elevated aldosterone levels despite high Na intake. Marine birds are excellent examples of physiological plasticity.
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effect of cadmium on pekin duck total body water water flux renal filtration and Salt Gland function
Journal of Toxicology and Environmental Health, 2000Co-Authors: Darin C. Bennett, Maryanne R. Hughes, John E Elliott, A M Scheuhammer, Judit E G SmitsAbstract:The following hypotheses were examined using Pekin ducks (Anas platyrhynchos) as a model for marine ducks: cadmium (Cd) intake affects (1) Salt Gland and/or kidney function of ducks and (2) osmoregulation differently in male and female ducks. Birds were fed 0, 50, or 300 microg Cd/g food. They were gradually acclimated to 450 mM NaCl and then drank 300 mM NaCl for 3 mo while Salt Gland secretion (SGS), glomerular filtration rate (GFR), total body water (TBW), and water flux (WF) were measured in ducks eating control and high-Cd diets. Cadmium ingestion did not markedly affect body mass, but significantly enlarged the Salt Glands and kidneys. Enhancement of kidney mass was greater in males. Cadmium ingestion did not affect TBW or WF, but tended to increase interstitial fluid space at the expense of intracellular fluid. Sex did not affect TBW, but males had greater WF. Birds that ate Cd diets, especially the higher Cd diet, exhibited renal tubular damage and lower GFR. Ducks that ate Cd had lower plasma sodium concentration and osmolality and, to activate SGS, required longer infusion of NaCl and larger increments
Trevor J Shuttleworth - One of the best experts on this subject based on the ideXlab platform.
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vasoactive intestinal peptide stimulates a camp mediated cl current in avian Salt Gland cells
Regulatory Peptides, 1994Co-Authors: Shaun C Martin, Trevor J ShuttleworthAbstract:Abstract VIP plays an integral role in both protein and fluid secretion in many exocrine Glands. By employing the perforated patch-clamp whole-cell recording technique we investigated the effects of VIP on membrane potential and transmembrane currents in avian exocrine Salt Gland cells. Prior to application of VIP, Salt Gland cells had a resting membrane potential close to −45 mV. When challenged with VIP (1–100 nM) a sustained depolarization to E Cl − was induced which was mimicked by the application of cell-permeable cAMP analogues or forskolin (1 μM). By employing the voltage-clamp recording configuration a sustained increase in current was observed with a reversal potential which approximated E Cl − . Ionic substitution experiments confirmed that the current was a Cl− conductance which was inhibited by the Cl− channel blockers flufenamic acid and niflumic acid and by the inhibitory cAMP isomer, adenosine-3′,5′-cyclic monophosphothioate, Rp-isomer. Based on this, and the fact that the kinetic properties of the Cl− current activated by VIP are similar to those activated by cAMP, we propose that VIP-receptor interaction results in the activation of a cAMP-dependent Cl− current.
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muscarinic receptor activation stimulates oscillations in k and cl currents which are acutely dependent on extracellular ca2 in avian Salt Gland cells
Pflügers Archiv: European Journal of Physiology, 1994Co-Authors: Shaun C Martin, Trevor J ShuttleworthAbstract:By utilizing the perforated-patch variant of the whole-cell patch-clamp recording technique, in order to maintain the integrity of the normal cellular buffering systems, we demonstrate that carbachol (CCh) stimulates simultaneous oscillations in a Ca2+- and voltageactivated K+ current and a linear Ca2+-activated Cl− current in an exocrine avian Salt Gland cell preparation. Similar conductance changes, although sustained rather than oscillatory, are stimulated by the Ca2+ ionophore A23187. The outward K+ current can be inhibited by tetraethylammonium chloride (TEA) whereas the Cl− current is inhibited by the Cl− channel blockers 5-nitro-2-(3-phenylpropylamino) (NPPB) and N-phenylanthranilic acid (DPC). The oscillations in current stimulated by CCh are acutely dependent on extracellular Ca2+ and are not affected by the application of low doses of caffeine. In addition, the application of caffeine at all doses fails to mimic the current transients stimulated by CCh. As both caffeine and A23187 are unable to stimulate oscillations under the perforated-patch conditions we suggest that in avian Salt Gland cells the primary oscillatory mechanism probably involves a one-pool mechanism of Ca2+ release which is intimately related to the activation of a Ca2+ influx pathway.
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Muscarinic-receptor activation stimulates oscillations in K^+ and Cl^− currents which are acutely dependent on extracellular Ca^2+ in avian Salt Gland cells
Pflügers Archiv, 1994Co-Authors: Shaun C Martin, Trevor J ShuttleworthAbstract:By utilizing the perforated-patch variant of the whole-cell patch-clamp recording technique, in order to maintain the integrity of the normal cellular buffering systems, we demonstrate that carbachol (CCh) stimulates simultaneous oscillations in a Ca^2+- and voltageactivated K^+ current and a linear Ca^2+-activated Cl^− current in an exocrine avian Salt Gland cell preparation. Similar conductance changes, although sustained rather than oscillatory, are stimulated by the Ca^2+ ionophore A23187. The outward K^+ current can be inhibited by tetraethylammonium chloride (TEA) whereas the Cl^− current is inhibited by the Cl^− channel blockers 5-nitro-2-(3-phenylpropylamino) (NPPB) and N -phenylanthranilic acid (DPC). The oscillations in current stimulated by CCh are acutely dependent on extracellular Ca^2+ and are not affected by the application of low doses of caffeine. In addition, the application of caffeine at all doses fails to mimic the current transients stimulated by CCh. As both caffeine and A23187 are unable to stimulate oscillations under the perforated-patch conditions we suggest that in avian Salt Gland cells the primary oscillatory mechanism probably involves a one-pool mechanism of Ca^2+ release which is intimately related to the activation of a Ca^2+ influx pathway.
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A G_q-type G protein couples muscarinic receptors to inositol phosphate and calcium signaling in exocrine cells from the avian Salt Gland
The Journal of Membrane Biology, 1993Co-Authors: Jan-peter Hildebrandt, Trevor J ShuttleworthAbstract:Muscarinic acetylcholine receptor (mAChR) activation in isolated cells from the nasal Salt Gland of the domestic duck ( Anas platyrhynchos ) results in a rapid increase in the rate of phosphatidylinositol hydrolysis and pronounced intracellular calcium signals. Both responses can be elicited by treating these cells with fluoroaluminate (AlF _4 ^− ) indicating the involvement of a heterotrimeric G protein in the transmembrane signaling process. To characterize this G protein, electrophoretically separated membrane proteins were blotted onto nitrocellulose filters and probed with peptide-antibodies raised against portions of different α-subunits of mammalian G proteins. We could demonstrate the presence of at least four different G proteins in Salt Gland cell membranes. Two of these proteins (40 and 41 kD) were ADP-ribosylated by pertussis toxin and were recognized by an antiserum against a common sequence in all G protein α-subunits. One protein (46 kD) was a cholera toxin-substrate and was recognized by a G_s-specific antiserum; the other (42 kD) was recognized by G_q-specific antisera and was resistant to ADP-ribosylation. Since the initial inositol phosphate production upon receptor activation with carbachol and the resulting calcium signals were not affected by pertussis toxin-pretreatment of Salt Gland cells, we conclude that muscarinic receptors are coupled to phospholipase C by a G_q-type G protein.
Paul D. Cooper - One of the best experts on this subject based on the ideXlab platform.
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Control of Salt Gland activity in the hatchling green sea turtle, Chelonia mydas.
Journal of comparative physiology. B Biochemical systemic and environmental physiology, 2000Co-Authors: Richard D. Reina, Paul D. CooperAbstract:We studied the control of Salt Gland secretion in hatchling Chelonia mydas. The threshold Salt load to activate Salt secretion was between 400 μmol NaCl 100 g bodymass (BM)−1 and 600 μmol NaCl 100 g BM−1, which caused an increase in plasma sodium concentration of 13% to 19%. Following a Salt load of 2700 μmol NaCl 100 g BM−1, Salt Gland secretion commenced in 12 ± 1.3 min and reached maximal secretory concentration within 2–7 min. Maximal secretory rate of a single Gland averaged 415 μmol Na 100 g BM−1 h−1. Plasma sodium concentration and total osmotic concentration after Salt loading were significantly higher than pretreatment values within 2 min. Adrenalin (25 μg kg BM−1) and the cholinergic agonist methacholine (1 mg kg BM−1) inhibited Salt Gland activity. Atropine (10 mg kg BM−1) reversed methacholine inhibition and stimulated Salt Gland secretion when administered with a subthreshold Salt load. Arginine vasotocin produced a transient reduction in sodium secretion by the active Gland, while atrial natriuretic factor, vasoactive intestinal peptide and neuropeptide Y had no measurable effect on any aspect of Salt Gland secretion. Our results demonstrated that secretion of the Salt Gland in C. mydas can be modified by neural and hormonal chemicals in vivo and that the cholinergic and adrenergic stimulation of an exocrine Gland do not appear to have the typical, antagonist actions on the chelonian Salt Gland.
Rudiger Gerstberger - One of the best experts on this subject based on the ideXlab platform.
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localization of nadph diaphorase activity in the Salt Gland of the Saltwater acclimated pekin duck
Neuroscience Letters, 1995Co-Authors: Thomas Hubschle, Karlheinz Kortje, Rudiger GerstbergerAbstract:Exocrine secretion of the avian Salt Gland is controlled by the autonomic nervous system. NADPH-diaphorase histochemistry was employed at the light and electron microscopic level to provide the morphological basis for a putative nitrergic regulation of Salt Gland function. NADPH-diaphorase staining was localized in two cell populations of the parasympathetic secretory ganglion at high cell density and equal distribution throughout the ganglionic mass. In addition, Salt Gland-intrinsic neurons, arranged in small clusters and associated with major nitrergic fiber bundles, proved to be NADPH-diaphorase positive. These postganglionic nerve fibers innervated the secretory parenchyma in close proximity to the basal membrane of single secretory tubules as well as arterioles. The findings suggest participation of the nitrergic pathway in the autonomic control of avian Salt Gland function.
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partial uncoupling of Salt Gland blood flow and secretion in the pekin duck anas platyrhynchos
The Journal of Physiology, 1991Co-Authors: Rudiger GerstbergerAbstract:1. The aim of this study was to investigate the relationship between the blood flow through and the secretion by the Salt Glands of conscious, Salt-water-adapted Pekin ducks. 2. Intravenous loading with hypertonic saline induced a steady-state secretion from the Salt Glands with a concomitant increase in whole-organ blood flow. The distribution of elevated local Glandular blood flow was, however, uneven and in addition demonstrated vasomotor patterns that ranged from constant to rhythmic. 3. During on-going Salt Gland secretion, the infusion of three vasoactive agents, 5Val-angiotensin II (ANG II), 8Arg-vasotocin (AVT) and noradrenaline, via the carotid artery had differential effects on Salt Gland blood flow and secretion. 4. ANG II (80 pmol min-1 (kg body wt)-1) had no effect on mean arterial blood pressure (MABP), produced a transient 30% decrease in Glandular blood flow and strongly diminished Salt Gland secretion (retention of 6.4 mosmol NaCl). 5. AVT (20 pmol min-1 (kg body wt)-1) had no effect on MABP and did not alter Salt Gland secretion despite a 35% reduction in blood flow. 6. Noradrenaline (20 nmol min-1 (kg body wt)-1) elevated MABP by 15 mmHg, reduced Salt Gland blood flow by more than 50%, but diminished Salt Gland secretion only slightly (retention of 2.7 mosmol NaCl). 7. Using ANG II, AVT and noradrenaline as hormonal tools, integrated changes in blood flow rate did not correspond with integrated changes in Salt Gland excretion. The partial dissociation between both parameters shows that control of secretion by the Salt Gland is more complex than simply being linearly dependent upon blood flow through it.
