Extrarenal Mechanisms in Hydromineral and Acid‐Base Regulation in Aquatic Vertebrates

Kirschner, Leonard B.

doi:10.1002/cphy.cp130109

Cited by 12 publications

(13 citation statements)

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“…2, A and B). Inhibition of CA would be expected to cause a simultaneous and equal inhibition of Na ϩ and Cl Ϫ uptake because, as outlined above, the activity of CA provides protons to the H ϩ -ATPase for apical uptake of Na ϩ and HCO 3 Ϫ for apical exchange with Cl Ϫ (13,18). Third, CA activity was inhibited by ϳ30% by 1 h of silver exposure (Fig.…”

Section: Discussionmentioning

confidence: 94%

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Time course analysis of the mechanism by which silver inhibits active Na⁺and Cl⁻uptake in gills of rainbow trout

Morgan¹,

Grosell²,

Gilmour³

et al. 2004

American Journal of Physiology-Regulatory, Integrative and Comp

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A time course analysis using (110m)Ag, (24)Na(+), and (36)Cl(-) examined gill silver accumulation and the mechanism by which waterborne silver (4.0 x 10(-8) M; 4.3 microg/l) inhibits Na(+) and Cl(-) uptake in gills of freshwater rainbow trout. Analyses of gill and body fluxes allowed calculation of apical uptake and basolateral export rates for silver, Na(+), and Cl(-). To avoid changes in silver bioavailability, flow-through conditions were used to limit the buildup of organic matter in the exposure water. For both Na(+) and Cl(-) uptake, apical entry, rather than basolateral export, was the rate-limiting step; Na(+) and Cl(-) uptake declined simultaneously and equally initially, with both uptakes reduced by approximately 500 nmol.g(-1).h(-1) over the 1st h of silver exposure. There was a further progressive decline in Na(+) uptake until 24 h. Carbonic anhydrase activity was inhibited by 1 h, whereas Na(+)-K(+)-ATPase activity was not significantly inhibited until 24 h of exposure. These results indicate that carbonic anhydrase inhibition can explain the early decline in Na(+) and Cl(-) uptake, whereas the later decline is probably related to Na(+)-K(+)-ATPase blockade. Contrary to previous reports, gill silver accumulation increased steadily to a plateau. Despite the rapid inhibition of apical Na(+) and Cl(-) uptake, apical silver uptake (and basolateral export) increased until 10 h, before decreasing thereafter. Thus silver did not inhibit its own apical uptake in the short term. These results suggest that reduced silver bioavailability is the mechanism behind the pattern of peak and decline in gill silver accumulation previously reported for static exposures to silver.

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Section: Discussionmentioning

confidence: 94%

“…In comparison, amiloride, the most widely used inhibitor of Na ϩ transport, must be presented at 10 Ϫ4 M to cause a 75-90% inhibition (see Ref. 18 for a review). Work to date has identified inhibition of basolateral membrane Na ϩ -K ϩ -ATPase activity as the mechanism by which silver blocks Na ϩ uptake in the trout gill (24).…”

mentioning

confidence: 99%

Time course analysis of the mechanism by which silver inhibits active Na⁺and Cl⁻uptake in gills of rainbow trout

Morgan¹,

Grosell²,

Gilmour³

et al. 2004

American Journal of Physiology-Regulatory, Integrative and Comp

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“…, Cl -, and K ? in a drink are taken in across the gut (Hickman 1968;Shehadeh and Gordon 1969;Kirschner 1997). Much of the Na ?…”

Section: Osmoregulation In Seawatermentioning

confidence: 99%

The physiology of hyper-salinity tolerance in teleost fish: a review

Gonzalez

2011

J Comp Physiol B

111

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Hyper-saline habitats (waters with salinity >35 ppt) are among the harshest aquatic environments. Relatively few species of teleost fish can tolerate salinities much above 50 ppt, because of the challenges to osmoregulation, but those that do, usually estuarine, euryhaline species, show a strong ability to osmoregulate in salinities well over 100 ppt. Typically, plasma Na(+) and Cl(-) concentrations rise slowly or not at all up to about 65 ppt. At higher salinities ion levels do rise, but the increase is small relative to the magnitude of increase in concentrations of the surrounding water. A number of adjustments are responsible for such strong osmoregulation. Reduced branchial water permeability is indicated by the observation that with the exposure to hyper-salinities drinking rates rise more slowly than the branchial osmotic gradient. Lower water permeability limits osmotic water loss and greatly reduces the salt load incurred in replacing it. Still, increased gut Na(+)/K(+)-ATPase (NAK) activity is necessary to absorb the larger gut salt load and increased HCO(3) (-) secretion is required to precipitate Ca(2+) and some Mg(2+) in the imbibed water to facilitate water absorption. All Na(+) and Cl(-) taken up must be excreted and increased branchial salt excreting capacity is indicated by elevated mitochondrion-rich cell density and size, gill NAK activity and expression of chloride channels. Excretion of Na(+) and Cl(-) occurs against a larger gradient than in seawater and calculation of the equilibrium potential for Na(+) across the gill epithelium indicates that the trans-epithelial potential required for excretion of Na(+) climbs with salinity up to about 65 ppt before leveling off due to the increasing plasma Na(+) levels. During acute transition to SW or mildly hyper-saline waters, some species have shown the ability to upregulate branchial NAK activity rapidly and this may play an important role in limiting disturbances at higher salinities. It does not appear that the opercular epithelium, which in SW acts in a way that is functionally similar to the gills, continues to do so in hyper-saline waters. Little is know about the hormones involved in acclimation to hyper-salinity, but the few studies available suggest a role for cortisol, but not growth hormone and insulin-like growth factor. Despite the increased transport capacity evident in both the gill and gut in hyper-saline waters there is no clear trend toward increased metabolic rate. These studies provide a general outline of the mechanisms of osmoregulation in these species, but significant questions still remain.

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“…The majority (Ͼ90%) of acid-base transfer between fish and the environment occurs across the gills and exposure to low environmental pH apparently causes acid loading by reducing branchial acid excretion (14,45 , likely contributed to the significant increase in serum osmolality (16 mosmol/kgH 2 O) during metabolic acidosis. NHEs subserve branchial acid excretion in teleosts, and increased branchial NHE activity during acidosis exacerbates the plasma Na ϩ load already experienced by marine teleosts (7,17). Urine osmolality, glomerular filtration rate (GFR), and urine flow rate were unchanged by acidosis.…”

Section: Influence Of Metabolic Acidosis On Somentioning

confidence: 99%

Stimulation of renal sulfate secretion by metabolic acidosis requires Na⁺/H⁺exchange induction and carbonic anhydrase

Pelis¹,

Edwards²,

Kunigelis³

et al. 2005

American Journal of Physiology-Renal Physiology

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2Ϫ secretion by the marine teleost renal proximal tubule was examined. Metabolic acidosis was mimicked in primary cultures of winter flounder renal proximal tubule epithelium (fPTCs) mounted in Ussing chambers by reducing interstitial pH to 7.1 (normally 7.7). fPTCs with metabolic acidosis secreted SO 4 2Ϫ at a net rate that was 40% higher than in paired isohydric controls (pH 7.7 on interstitium). The stimulation was completely blocked by the carbonic anhydrase inhibitor methazolamide (100 M). Although Na ϩ /H ϩ exchange (NHE) isoforms 1, 2, and 3 were identified in fPTCs by immunoblotting, administering EIPA (20 M) to the interstitial and luminal bath solutions had no effect on net SO 4 2Ϫ secretion by fPTCs with a normal interstitial pH of 7.7. However, EIPA (20 M) blocked most of the stimulation caused by acidosis when applied to the lumen but not interstitium, demonstrating that induction of brush-border NHE activity is important. In the intact flounder, serum pH dropped 0.4 pH units (pH 7.7 to 7.3, at 2-3 h) when environmental pH was lowered from 7.8 to ϳ4. (4,6,28). NHE activity has been demonstrated in renal brush-border membrane vesicles from seawater adapted eels (Anguilla anguilla) and NHE isoform 3 (NHE3) mRNA has been identified in the kidneys of the acidtolerant Osorezan dace (Tribolodon hakonensis) (15,43,48). Although there is evidence suggesting that NHE is present in the marine teleost kidney, low urine flow rates appear to preclude a significant renal participation in acid/base balance (8,20).Metabolic acidosis manifests as a decrease in serum pH and [HCO 3 Ϫ ] without a change in PCO 2 . The overproduction of acid (e.g., lactic acid), ingestion of acid, and interference with branchial acid excretion (e.g., exposure of fish to acidic water) can all elicit metabolic acidosis. In rats, metabolic acidosis (Ͼ24 h) increases renal SO 4 2Ϫ excretion by effectively reducing Na-dependent SO 4 2Ϫ reabsorption (29). The purpose of the current study was to determine the short-term effect of metabolic acidosis and the role of NHE activity in proximal tubular SO 4 2Ϫ secretion. The findings reported here indicate that metabolic acidosis acutely stimulates the rate of renal proximal tubular SO 4 2Ϫ secretion both in vitro and in vivo. Furthermore, both CA and brush-border NHE activity appear to be required for the high level of SO 4 2Ϫ secretion during acidosis.

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Extrarenal Mechanisms in Hydromineral and Acid‐Base Regulation in Aquatic Vertebrates

Abstract: The sections in this article are: Physical Background Dissipative Flows Hyperosmotic Regulation Reducing Dissipative Flows Compensatory Flows: Water Compensatory Flows: Active Ion Absorption The Frog Skin Model: Symmetric Solutions and Voltage Clamp … Show more

Cited by 12 publications

References 289 publications

Time course analysis of the mechanism by which silver inhibits active Na⁺and Cl⁻uptake in gills of rainbow trout

Time course analysis of the mechanism by which silver inhibits active Na⁺and Cl⁻uptake in gills of rainbow trout

The physiology of hyper-salinity tolerance in teleost fish: a review

Stimulation of renal sulfate secretion by metabolic acidosis requires Na⁺/H⁺exchange induction and carbonic anhydrase

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Extrarenal Mechanisms in Hydromineral and Acid‐Base Regulation in Aquatic Vertebrates

Abstract: The sections in this article are: Physical Background Dissipative Flows Hyperosmotic Regulation Reducing Dissipative Flows Compensatory Flows: Water Compensatory Flows: Active Ion Absorption The Frog Skin Model: Symmetric Solutions and Voltage Clamp … Show more

Cited by 12 publications

References 289 publications

Time course analysis of the mechanism by which silver inhibits active Na+and Cl−uptake in gills of rainbow trout

Time course analysis of the mechanism by which silver inhibits active Na+and Cl−uptake in gills of rainbow trout

The physiology of hyper-salinity tolerance in teleost fish: a review

Stimulation of renal sulfate secretion by metabolic acidosis requires Na+/H+exchange induction and carbonic anhydrase

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Time course analysis of the mechanism by which silver inhibits active Na⁺and Cl⁻uptake in gills of rainbow trout

Time course analysis of the mechanism by which silver inhibits active Na⁺and Cl⁻uptake in gills of rainbow trout

Stimulation of renal sulfate secretion by metabolic acidosis requires Na⁺/H⁺exchange induction and carbonic anhydrase