Active urea transport independent of H+ and Na+ transport in frog skin epithelium

Lacoste, Isabelle; Dunel‐Erb, Suzanne; Harvey, Bill; Laurent, P.; Ehrenfeld, Jordi

doi:10.1152/ajpregu.1991.261.4.r898

Cited by 10 publications

(10 citation statements)

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“…Physiological evidence for active urea transport has been reported in mammalian kidney (reviewed by Sands 2003), amphibian kidney (SchmidtNielsen and Shrauger 1963) and skin (Garcia-Romeu et al 1981;Rapoport et al 1988;Lacoste et al 1991), elasmobranch kidney (S. acanthias; Schmidt-Nielsen et al 1972;Morgan et al 2003b) and gill Fines et al 2001), and teleost kidney (O. mykiss: McDonald andWood 1998, 2003;O. beta: McDonald et al 2000;P.…”

Section: Introductionmentioning

confidence: 99%

Greatly Elevated Urea Excretion after Air Exposure Appears to Be Carrier Mediated in the Slender Lungfish (Protopterus dolloi)

Wood¹,

Walsh²,

Chew³

et al. 2005

Physiological and Biochemical Zoology

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Under aquatic conditions, Protopterus dolloi is ammoniotelic, excreting only small amounts of urea-N. However, upon return to water after 30 d estivation in air, the lungfish excretes only small amounts of ammonia-N but massive amounts of urea-N. A similar pattern is seen after 21-30 d of terrestrialization, a treatment in which the lungfish is air exposed but kept moist throughout. After both treatments, the time course of urea-N excretion is biphasic with an immediate increase, then a fall, and finally a second larger increase that peaks at about 12 h and may be prolonged for several days thereafter. Urea-N excretion rates during the second peak reach 2,000-6,000 micromol N kg(-1) h(-1), two to three orders of magnitude greater than rates in most fish and comparable only to rates in species known to employ UT-A type facilitated diffusion urea transporters. Divided chamber studies and measurements of the clearance rates of [3H]-PEG-4000 (a glomerular filtration and paracellular diffusion marker) and two structural analogs of urea ([14C]-acetamide and [14C]-thiourea) were performed to characterize the two peaks of urea-N excretion. The smaller first peak was almost equally partitioned between the head (including internal and external gills) and the body compartment (including urinary opening), was accompanied by only a modest increase in [14C]-acetamide clearance equal to that in [14C]-thiourea clearance, and could be accounted for by a large but short-lasting increase in [3H]-PEG-4000 clearance (to about fivefold the terrestrial rate). The delayed, much larger second peak in urea-N excretion represented an elevated efflux into both compartments but occurred mainly (72%) via the body rather than the head region. This second peak was accompanied by a substantial increase in [14C]-acetamide clearance but only a modest further rise in [14C]-thiourea clearance. The acetamide to thiourea permeability ratio was typical of UT-A type transporters in other fish. [3H]-PEG-4000 clearance was stable at this time at about double the terrestrial rate, and excretion rates of urea and its analogs were many fold greater than could be accounted for by [3H]-PEG-4000 clearance. We conclude that the first peak may be explained by elevated urinary excretion and paracellular diffusion across the gills upon resubmergence, while the second peak is attributable to a delayed and prolonged activation of a UT-A type facilitated diffusion mechanism, primarily in the skin and perhaps also in branchial epithelia.

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Section: Introductionmentioning

confidence: 99%

Greatly Elevated Urea Excretion after Air Exposure Appears to Be Carrier Mediated in the Slender Lungfish (Protopterus dolloi)

Wood¹,

Walsh²,

Chew³

et al. 2005

Physiological and Biochemical Zoology

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“…Substantial evidence exists, however, for active or facilitated urea transport across a variety of tissues in elasmobranchs, amphibians, and mammals (e.g., Schmidt-Nielsen and Rabinowitz 1964; Levine et al 1973;Kaplan et al 1974;Curci et al 1976;Hays et al 1977;Katz et al 1981;Brahm 1983;Chou and Knepper 1989;Effros et al 1992). In some amphibians, active urea uptake mechanisms in the skin aid retention of elevated internal urea levels (Katz et al 1981;Rapoport et al 1989;Lacoste et al 1991). It is not known whether a specialized urea transport protein exists in gill epithelial membranes.…”

Section: Introductionmentioning

confidence: 99%

Ammonia and urea excretion in the tidepool sculpin (Oligocottus maculosus): sites of excretion, effects of reduced salinity and mechanisms of urea transport

Wright

Pärt

Wood

1995

Fish Physiol Biochem

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Tidepool sculpins live in a variable environment where water temperature, salinity, gas tensions, and pH can change considerably with the daily tide cycle. Tidepool sculpins are primarily ammoniotelic, with 8-17% of nitrogen wastes excreted as urea. The majority of net ammonia (J(net) amm; 85%) and urea (J(net) urea; 74%) excretion occurred across the gill, with the remainder excreted across the skin, the kidney, and/or gut. Acute (2h) exposure to 50% seawater significantly increased J(net) urea (2.8-fold), but reduced J(net) amm (3.5-fold). In fish exposed to 50% seawater for 1 week, J(net) urea returned to control values, but J(net) amm remained slightly depressed. Unidirectional urea influx (J(in) urea) and efflux (J(out) urea) were measured using(14)C-urea to determine if urea was excreted across the gills by simple diffusion or by a carrier-mediated mechanism. J(in) urea increased in a linear manner with increasing urea water levels (0-11 mmol N l(-1)), while J(out) urea was independent of external urea concentrations. As well, J(net) urea and J(out inurea) were not significantly different from one another, indicating the absence of "back transport". Urea analogs and transport inhibitors added to the water did not have any consistent effect on unidirectional urea flux. These results demonstrate that ammonia and urea excretion rates and sites of excretion in tidepool sculpins are very similar to those found in other marine and freshwater teleosts. Urea and ammonia may play a role in osmoregulation as excretion rates and tissue levels were influenced by changes in water salinity. Finally, we found no evidence for a specific urea carrier; branchial urea excretion is likely dependent on simple diffusion.

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“…The combination of sodium dependence and phloretin insensitivity differentiate this rat initial IMCD net urea transporter from all previously described active urea transport processes (19)(20)(21)(22)(23)(24). Table I summarizes the characteristics of previously described active urea transport processes.…”

Section: Discussionmentioning

confidence: 86%

Sodium-dependent net urea transport in rat initial inner medullary collecting ducts.

Isozaki¹,

Lea²,

Tumlin³

et al. 1994

J. Clin. Invest.

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We reported that feeding rats 8% protein for 3 wk induces net urea transport and morphologic changes in initial inner medullary collecting ducts (IMCDs) which are not present in rats fed 18% protein. In this study, we measured net urea transport in microperfused initial IMCDs from rats fed 8% protein for -3 wk and tested the effect of inhibiting Na+/ K+-ATPase activity and found that adding 1 mM ouabain to the bath reversibly inhibited net urea transport from 14+3 to 6±2 pmol/mm per min (P < 0.01), and that replacing potassium (with sodium) in the bath reversibly inhibited net urea transport from 18±3 to 5±0 pmol/mm per min (P < 0.01). Replacing perfusate sodium with N-methyl-Dglucamine reversibly inhibited net urea transport from 12±2 to 0±1 pmol/mm per min (P < 0.01), whereas replacing bath sodium had no significant effect on net urea transport. Adding 10 nM vasopressin to the bath exerted no significant effect on net urea transport. Finally, we measured Na+/K+-ATPase activity in initial and terminal IMCDs from rats fed 18% or 8% protein and found no significant difference in either subsegment. Thus, net urea transport in initial IMCDs from rats fed 8% protein for 2 3 wk requires sodium in the lumen, is reduced by inhibiting Na+/K+-ATPase, and is unchanged by vasopressin or phloretin. These results suggest that net urea transport may occur via a novel, secondary active, sodium-urea cotransporter. (J.

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Active urea transport independent of H+ and Na+ transport in frog skin epithelium

Cited by 10 publications

References 0 publications

Greatly Elevated Urea Excretion after Air Exposure Appears to Be Carrier Mediated in the Slender Lungfish (Protopterus dolloi)

Greatly Elevated Urea Excretion after Air Exposure Appears to Be Carrier Mediated in the Slender Lungfish (Protopterus dolloi)

Ammonia and urea excretion in the tidepool sculpin (Oligocottus maculosus): sites of excretion, effects of reduced salinity and mechanisms of urea transport

Sodium-dependent net urea transport in rat initial inner medullary collecting ducts.

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