Low protein diet alters urea transport and cell structure in rat initial inner medullary collecting duct.

Isozaki, Taisuke; Verlander, Jill W.; Sands, Jeff M.

doi:10.1172/jci116852

Cited by 52 publications

(69 citation statements)

References 39 publications

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“…No significant difference was found between DM and CO rat mellitus is different because the changes in UT mRNA and protein abundance observed in diabetes mellitus differ from those resulting from protein-rich diet (unchanged mRNA [40], and decreased 117000 M r isoform [31]). In contrast, some of the diabetes-induced changes resemble those induced by chronic low protein feeding, such as extension of UT-A1 mRNA [41] and vasopressin-dependent urea permeability [33,42] to the initial part of the IMCD, increase in the 117000 M r isoform [31], and lack of change in UT-A2 and UT-B1 mRNA abundance [40].…”

Section: Discussionmentioning

confidence: 96%

Aquaporin-2 and urea transporter-A1 are up-regulated in rats with Type I diabetes mellitus

et al. 2001

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In diabetes mellitus, water turnover in the body is enhanced because of the glucose-induced osmotic diuresis and it is usually assumed that the concentrating capacity of the kidney is partially impaired. On the other hand, plasma vasopressin concentration is known to be increased by several fold in patients with Type I (insulin-dependent) diabetes mellitus or Type II (non-insulin-dependent) diabetes mellitus as well as in animal models of experimental or genetic diabetes mellitus [1±6]. This high vasopressin concentration is accompanied by a desensitization of V1 a receptors in liver, kidney and platelets [7,8]. In contrast, renal V2 receptors, responsible for the antidiuretic action of the hormone, are not down-regulated [8].Actually, higher vasopressin in diabetes mellitus probably represents an appropriate adaptation by limiting to some extent the amount of water required Abstract Aims/hypothesis. Although the urine flow rate is considerably higher in diabetes mellitus, water reabsorption is greatly increased to concentrate an increased amount of solutes. Our study evaluated the expression of aquaporins and urea transporters, which are essential to the urinary concentration process. Methods. Northern blot and immunoblot were used to quantify mRNA and proteins for aquaporin-2 (AQP2) as well as urea transporters UT-A1, UT-A2 and UT-B1, in subzones of the renal medulla of rats with streptozotocin-induced diabetes. Results. In these rats, glycaemia, urine flow rate and water reabsorption were respectively fourfold, ninefold and fourfold those of control rats. The AQP2 protein isoforms were significantly up-regulated in outer and inner medulla. In the base and tip of inner medulla, UT-A1 mRNA was significantly up-regulated (three-and 1.3-fold, respectively) as well as the 117 kD protein (ten-and threefold, respectively) whereas the 97 kD protein was not changed or decreased twofold, respectively. This suggests that, in diabetes, the inner medullary collecting duct is endowed with more UT-A1, especially in its initial part. In the case of mRNA and proteins of UT-A2, located in thin descending limbs in the inner stripe of outer medulla, they were respectively not changed and down-regulated in diabetic rats. Conclusion/interpretation. This study shows that in diabetes, the increased expression of AQP2 and UT-A1 in medullary collecting duct is consistent with an improved concentrating activity. In addition, the underexpression of UT-A2 and the overexpression of UT-A1 in the initial medullary collecting duct are reminiscent of the changes seen after experimental reduction of urine concentration or low protein feeding. [Diabetologia (2001) 44: 637±645]

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Section: Discussionmentioning

confidence: 96%

Aquaporin-2 and urea transporter-A1 are up-regulated in rats with Type I diabetes mellitus

et al. 2001

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“…Schmidt-Nielsen and colleagues first demonstrated the existence of active urea reabsorption which is coupled to sodium reabsorption in the kidney of the spiny dogfish, Squalus acanthias (16). We showed that urea is actively reabsorbed via a secondary active, sodium-coupled cotransport process in the rat initial IMCD (IMCD 1 ) from rats fed a low-protein diet for 3 wk (9)(10)(11). We also showed that urea is actively secreted via a secondary active, sodium-coupled countertransport process in the deepest portion of the rat terminal IMCD, the IMCD 3 , but not in the middle third of the IMCD, the IMCD 2 , nor in the initial IMCD of rats fed a normal diet (12).…”

Section: Introductionmentioning

confidence: 91%

“…To study active urea transport, tubules were perfused with the same perfusate and bath solution (except during the ion substitution studies described below) whose composition was identical to the dissection solution (described above) except that 3 mM urea was added to the solution (9,10,12). To calculate J urea , V o is assumed to be equal to V l , because there is no osmotic gradient across the tubule and hence, no driving force for water reabsorption.…”

Section: Protocolsmentioning

confidence: 99%

“…In addition to facilitated urea transport, there is evidence for active urea transport process(es) in the kidney of rat (9)(10)(11)(12), rabbit (13), dog (14,15), spiny dogfish (16), and human (17). Schmidt-Nielsen and colleagues first demonstrated the existence of active urea reabsorption which is coupled to sodium reabsorption in the kidney of the spiny dogfish, Squalus acanthias (16).…”

Section: Introductionmentioning

confidence: 99%

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Active sodium-urea counter-transport is inducible in the basolateral membrane of rat renal initial inner medullary collecting ducts.

Kato¹,

Sands²

1998

J. Clin. Invest.

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Rat inner medullary collecting ducts (IMCD 3 s) possess a luminal Na ϩ -dependent, active urea secretory transport process, which is upregulated by water diuresis. In this study of perfused IMCDs microdissected from base (IMCD 1 ), middle (IMCD 2 ), or tip (IMCD 3 ) of the inner medulla, we tested whether furosemide diuresis alters active urea transport. Rats received furosemide (10 mg/d s.c. for 3-4 d) and were compared with pair-fed control rats. Furosemide significantly decreased urine osmolality and urea clearance, and increased blood urea nitrogen. IMCD 3 s from furosemidetreated rats had significantly lower rates of active urea secretion than IMCD 3 s from control rats. IMCD 2 s showed no active urea transport in control or furosemide-treated rats.

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“…UT-A) and secondary active Na + /urea counter-transport systems (Chou and Knepper, 1989;Isozaki et al, 1993;Isozaki et al, 1994a;Isozaki et al, 1994b;Sands et al, 1996;Kato and Sands, 1998a;Kato and Sands, 1998b), but not Na + /urea cotransporters, and because water with a salinity of 1 contained ~15mmoll -1 Na + , which was higher than the normal intracellular Na + concentration (10mmoll -1 ), the possibility of a Na + /urea counter-transporter being expressed in the apical membrane of the buccopharyngeal epithelial cells of P. sinensis cannot be eliminated at present. However, active buccopharyngeal urea excretion resulted in extraordinarily high urea concentrations (~614mmoll -1 ) in the saliva of turtles injected intraperitoneally with urea; therefore, the possibility of the presence of a novel active urea transporter independent of Na + movement in the apical surface of the buccopharyngeal epithelium cannot be ignored.…”

Section: The Buccopharyngeal Epithelium Is Capable Of Active Urea Excmentioning

confidence: 97%

The Chinese soft-shelled turtle,Pelodiscus sinensis, excretes urea mainly through the mouth instead of the kidney

Loong

Lee

et al. 2012

Journal of Experimental Biology

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SUMMARY The Chinese soft-shelled turtle, Pelodiscus sinensis, is well adapted to aquatic environments, including brackish swamps and marshes. It is ureotelic, and occasionally submerges its head into puddles of water during emersion, presumably for buccopharyngeal respiration. This study was undertaken to test the hypothesis that the buccophyaryngeal cavity constitutes an important excretory route for urea in P. sinensis. Results indicate that a major portion of urea was excreted through the mouth instead of the kidney during immersion. When restrained on land, P. sinensis occasionally submerged their head into water (20–100 min), during which urea excretion and oxygen extraction occurred simultaneously. These results indicate for the first time that buccopharyngeal villiform processes (BVP) and rhythmic pharyngeal movements were involved in urea excretion in P. sinensis. Urea excretion through the mouth was sensitive to phloretin inhibition, indicating the involvement of urea transporters (UTs). In addition, saliva samples collected from the buccopharyngeal surfaces of P. sinensis injected intraperitoneally with saline contained ~36 mmol N l−1 urea, significantly higher than that (~2.4 mmol N l−1) in the plasma. After intraperitoneal injection with 20 μmol urea g−1 turtle, the concentration of urea in the saliva collected from the BVP increased to an extraordinarily high level of ~614 μmol N ml−1, but the urea concentration (~45 μmol N ml−1) in the plasma was much lower, indicating that the buccopharyngeal epithelium of P. sinensis was capable of active urea transport. Subsequently, we obtained from the buccopharyngeal epithelium of P. sinensis the full cDNA sequence of a putative UT, whose deduced amino acid sequence had ~70% similarity with human and mouse UT-A2. This UT was not expressed in the kidney, corroborating the proposition that the kidney had only a minor role in urea excretion in P. sinensis. As UT-A2 is known to be a facilitative urea transporter, it is logical to deduce that it was localized in the basolateral membrane of the buccopharyngeal epithelium, and that another type of primary or secondary active urea transporter yet to be identified was present in the apical membrane. The ability to excrete urea through the mouth instead of the kidney might have facilitated the ability of P. sinensis and other soft-shelled turtles to successfully invade the brackish and/or marine environment.

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Low protein diet alters urea transport and cell structure in rat initial inner medullary collecting duct.

Cited by 52 publications

References 39 publications

Aquaporin-2 and urea transporter-A1 are up-regulated in rats with Type I diabetes mellitus

Aquaporin-2 and urea transporter-A1 are up-regulated in rats with Type I diabetes mellitus

Active sodium-urea counter-transport is inducible in the basolateral membrane of rat renal initial inner medullary collecting ducts.

The Chinese soft-shelled turtle,Pelodiscus sinensis, excretes urea mainly through the mouth instead of the kidney

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