Journal articles on the topic 'Renal medullla'
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Ukey, Rahul Kisan, Reshma Baburao Shinde, Anil Shivshankar Rahule, Prafulla Nikam, and C. V. Diwan. "HISTOGENESIS OF HUMAN FETAL RENAL MEDULLA." International Journal of Anatomy and Research 6, no. 3.2 (August 10, 2018): 5544–49. http://dx.doi.org/10.16965/ijar.2018.277.
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Grossman, E. B., and S. C. Hebert. "Renal inner medullary choline dehydrogenase activity: characterization and modulation." American Journal of Physiology-Renal Physiology 256, no. 1 (January 1, 1989): F107—F112. http://dx.doi.org/10.1152/ajprenal.1989.256.1.f107.
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Betaine belongs to the trimethylamine class of osmolytes (osmotically active substances believed to play an important role in cell volume homeostasis) and has recently been identified in the inner medulla of the mammalian kidney. Trimethylamines accumulate in the renal inner medulla during hypertonic stress, and betaine content in the inner medulla has been shown recently to increase during hypernatremia, yet the mechanisms governing the modulation of trimethylamine content and, in particular, of betaine content are not well understood. In this study, we demonstrate the presence of choline dehydrogenase activity in the renal inner medullas of three separate rat strains. Choline dehydrogenase is the enzyme that catalyzes the first of two successive oxidation steps in the biosynthetic conversion of choline to betaine. The presence of choline dehydrogenase activity in the inner medulla suggests that betaine accumulation in the inner medulla may result, at least in part, through in situ synthesis. The Km and Vmax of the reaction in the inner medullas of Long-Evans rats are 4.7 +/- 0.5 mM and 36.9 +/- 5.0 nmol.mg protein-1.min-1, respectively. These values are similar to the characteristics of choline dehydrogenase in mammalian liver. During hypernatremia, when betaine content of the inner medulla has been shown to increase 1.5-fold, choline dehydrogenase activity remains unchanged (or slightly increased), whereas enzyme activity in the cortex increases approximately 50%. Possible mechanisms of inner medullary betaine accumulation are discussed.
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Veuthey, Tania, María Cecilia D'Anna, and Marta Elena Roque. "Role of the kidney in iron homeostasis: renal expression of Prohepcidin, Ferroportin, and DMT1 in anemic mice." American Journal of Physiology-Renal Physiology 295, no. 4 (October 2008): F1213—F1221. http://dx.doi.org/10.1152/ajprenal.90216.2008.
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It is known that renal tissue plays a role in normal iron homeostasis. The current study examines kidney function in iron metabolism under hemolytic anemia studying renal expression of Prohepcidin, Ferroportin (MTP1), and divalent metal transporter 1 (DMT1). The relationship between these proteins and iron pigments was also investigated. Immunohistochemical procedures to study renal expression of Prohepcidin, MTP1, and DMT1 were performed in healthy and anemic mice. Renal tissue iron was determined by Prussian blue iron staining. To assess anemia evolution and erythropoietic recovery, we used conventional tests. In healthy mice, Prohepcidin expression was marked in proximal tubules and inner medulla and absent in outer medulla. Cortical tissue of healthy mice also showed MTP1 immunostaining, mainly in the S2 segment of proximal tubules. Medullar tissue showed MTP1 expression in the inner zone. In addition, S2 segments showed intense DMT1 immunoreactivity with homogeneous DMT1 distribution throughout renal medulla. The main cortical findings in hemolytic anemia were in S2 segments of proximal tubules where we found that decreased Prohepcidin expression coincided with an increment in Ferroportin and DMT1 expression. This expression pattern was concomitant with increased iron in the same tubular zone. However, in medullar tissue both Prohepcidin and MTP1 decreased and DMT1 was detected mainly in larger diameter tubules. Our findings clearly demonstrate that in hemolytic anemia, renal Prohepcidin acts in coordination with renal Ferroportin and DMT1, indicating the key involvement of kidney in iron homeostasis when iron demand is high. Further research is required to learn more about these regulatory mechanisms.
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KIM, SOO WAN, SAM HYEON CHO, BONG SUK OH, CHUNG HO YEUM, KI CHUL CHOI, KYU YOUN AHN, and JONGUN LEE. "Diminished Renal Expression of Aquaporin Water Channels in Rats with Experimental Bilateral Ureteral Obstruction." Journal of the American Society of Nephrology 12, no. 10 (October 2001): 2019–28. http://dx.doi.org/10.1681/asn.v12102019.
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Abstract. Whether postobstructive diuresis could be related to altered regulation of aquaporin (AQP) water channels in the kidney was investigated. Male Sprague-Dawley rats underwent bilateral obstruction of the proximal ureters for 48 h. The renal expression of AQP1 to AQP4 proteins was then determined by Western blot and immunohistochemical analyses. For elucidation of the primary impairment in the upstream pathway leading to the expression of cAMP-mediated AQP channels, the expression of Gsαand that of adenylyl cyclase were also determined. For some rats, the obstruction was released for collection of urine samples. After the ureteral obstruction, the urinary flow rate was increased and free water reabsorption was decreased. In the obstructed kidneys, the expression of AQP1 to AQP3 was decreased in the cortex, outer medulla, and inner medulla, whereas that of AQP4 was decreased in the inner medulla. Immunoreactivities for AQP1 to AQP4 were also decreased in the obstructed kidneys. The protein expression of Gsαwas decreased in the cortex, outer medulla, and inner medulla, whereas that of adenylyl cyclase VI was decreased in the outer and inner medullae. cAMP generation stimulated by arginine vasopressin was decreased in the cortex, outer medulla, and inner medulla. cAMP generation in response to forskolin was decreased in the outer and inner medullae, whereas that in response to sodium fluoride was decreased in the cortex, outer medulla, and inner medulla. These results suggest that a reduced abundance of AQP water channels in the kidney accounts in part for postobstructive diuresis. The primary impairment of AQP channels that are regulated via the arginine vasopressin/cAMP pathway may lie at the level of G proteins and adenylyl cyclase itself.
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Jeon, Un Sil, Ki-Hwan Han, Soo-Hyun Park, Sang Do Lee, Mee Rie Sheen, Ju-Young Jung, Wan Young Kim, Jeff M. Sands, Jin Kim, and H. Moo Kwon. "Downregulation of renal TonEBP in hypokalemic rats." American Journal of Physiology-Renal Physiology 293, no. 1 (July 2007): F408—F415. http://dx.doi.org/10.1152/ajprenal.00502.2006.
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Hypokalemia causes a significant decrease in the tonicity of the renal medullary interstitium in association with reduced expression of sodium transporters in the distal tubule. We asked whether hypokalemia caused downregulation of the tonicity-responsive enhancer binding protein (TonEBP) transcriptional activator in the renal medulla due to the reduced tonicity. We found that the abundance of TonEBP decreased significantly in the outer and inner medullas of hypokalemic rats. Underlying mechanisms appeared different in the two regions because the abundance of TonEBP mRNA was lower in the outer medulla but unchanged in the inner medulla. Immunohistochemical examination of TonEBP revealed cell type-specific differences. TonEBP expression decreased dramatically in the outer and inner medullary collecting ducts, thick ascending limbs, and interstitial cells. In the descending and ascending thin limbs, TonEBP abundance decreased modestly. In the outer medulla, TonEBP shifted to the cytoplasm in the descending thin limbs. As expected, transcription of aldose reductase, a target of TonEBP, was decreased since the abundance of mRNA and protein was reduced. Downregulation of TonEBP appeared to have also contributed to reduced expression of aquaporin-2 and UT-A urea transporters in the renal medulla. In cultured cells, expression and activity of TonEBP were not affected by reduced potassium concentrations in the medium. These data support the view that medullary tonicity regulates expression and nuclear distribution of TonEBP in the renal medulla in cell type-specific manners.
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Burg, Maurice B., and Eugenia M. Peters. "Urea and methylamines have similar effects on aldose reductase activity." American Journal of Physiology-Renal Physiology 273, no. 6 (December 1, 1997): F1048—F1053. http://dx.doi.org/10.1152/ajprenal.1997.273.6.f1048.
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The concentration of urea in renal medullary cells is sufficiently high to inhibit activity of many enzymes, yet the cells survive and function. The generally accepted explanation is the counteracting osmolytes hypothesis, which holds that methylamines, such as glycerophosphorylcholine (GPC) and glycine betaine (betaine), found in the renal medulla stabilize biological macromolecules and oppose the effects of urea. The present study tests this hypothesis by determining the effects of urea and methylamines, singly and in combination, on the activity of aldose reductase, an enzyme that is important in renal medullas for catalyzing production of sorbitol from glucose. In apparent contradiction to the counteracting osmolytes hypothesis, urea (1.0 M) and three different methylamines (trimethylamine N-oxide, betaine, and GPC; 0.5 M) all have similar and partially additive inhibitory effects. They all decrease substantially both the Michaelis constant ( K m) and the maximum velocity ( V max). Also, a high concentration (0.5 M) of other organic osmolytes that are abundant in the renal medulla, namely inositol, sorbitol, or taurine, has a similar but lesser effect. KCl (0.3 M) causes a small increase in activity. We discuss the significance of these findings with regard to function of aldose reductase in the renal medulla and the counteracting osmolytes hypothesis.
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Armando, Ines, Miroslava Jezova, Augusto V. Juorio, José A. Terrón, Alicia Falcón-Neri, Cristina Semino-Mora, Hans Imboden, and Juan M. Saavedra. "Estrogen upregulates renal angiotensin II AT2receptors." American Journal of Physiology-Renal Physiology 283, no. 5 (November 1, 2002): F934—F943. http://dx.doi.org/10.1152/ajprenal.00145.2002.
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AT2 receptors may act in opposition to and in balance with AT1 receptors, their stimulation having beneficial effects. We found renal AT2receptor expression in female mice higher than in male mice. We asked the question of whether such expression might be estrogen dependent. In male, female, ovariectomized, and estrogen-treated ovariectomized mice, we studied renal AT1 and AT2 receptors by immunocytochemistry and autoradiography, AT2 receptor mRNA by RT-PCR, and cAMP, cGMP, and PGE2 by RIA. AT1receptors predominated. AT2 receptors were present in glomeruli, medullary rays, and inner medulla, and in female kidney capsule. AT1 and AT2 receptors colocalized in glomeruli. Female mice expressed fewer glomerular AT1receptors. Ovariectomy decreased AT1 receptors in medullary rays and capsular AT2 receptors. Estrogen administration normalized AT1 receptors in medullary rays and increased AT2 receptors predominantly in capsule and inner medulla, and also in glomeruli, medullary rays, and inner stripe of outer medulla. In medullas of estrogen-treated ovariectomized mice there was higher AT2 receptor mRNA, decreased cGMP, and increased PGE2 content. We propose that the protective effects of estrogen may be partially mediated through enhancement of AT2 receptor stimulation.
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Nakanishi, T., O. Uyama, and M. Sugita. "Osmotically regulated taurine content in rat renal inner medulla." American Journal of Physiology-Renal Physiology 261, no. 6 (December 1, 1991): F957—F962. http://dx.doi.org/10.1152/ajprenal.1991.261.6.f957.
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During antidiuresis renal medullary cells were previously found to accumulate large amounts of organic osmolytes, namely sorbitol, myo-inositol, glycerophosphorylcholine (GPC), and betaine. Large quantities of amino acids are also present in the renal medulla, but it has been questionable whether the levels of medullary amino acids are osmotically regulated. Therefore we directly measured 26 different amino acids, as well as sorbitol, myo-inositol, GPC, and betaine alone the corticomedullary axis of rats that were either salt loaded, after infusion of hypertonic NaCl solution, or were hydrated, after infusion of hypotonic NaCl solution. The amounts of sorbitol, myo-inositol, GPC, and betaine are greater in the inner medullas of salt-loaded rats compared with hydrated rats. In addition, the amount of taurine is much greater in the inner medullas of salt-loaded rats. Aspartic acid also increases in salt-loaded rats but to a lesser extent. There are substantial gradients of taurine, aspartic acid, and some of 24 other measured amino acids along the corticomedullary axis. However, taurine and aspartic acid are the only measured amino acids that increase significantly during salt loading.
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Aldekeeva, A. S., Y. S. Kraynova, E. D. Rudenko, and N. Z. Klyueva. "MARcKS and nAP-22 proteins mRnA expression in renal cortex and renal medulla of rats with spontaneous hypertension." "Arterial’naya Gipertenziya" ("Arterial Hypertension") 24, no. 4 (September 26, 2018): 435–40. http://dx.doi.org/10.18705/1607-419x-2018-24-4-435-440.
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Objective. To study the changes in mRNA expression level of two main protein kinase C substrates — MARCKS and NAP-22 — in rats with spontaneous hypertension (SHR rats) and in normotensive control rats (WKY rats) in renal cortex, renal medulla and total kidney. We also aimed at the identification of possible interstrain differences between the mRNA expression levels.Design and methods.We assessed the level of MARCKS and NAP-22 mRNA by real-time polymerase chain reaction in male SHR and WKY (as a normotensive control) rats.Results. In SHR rats, MARCKS mRNA expression level in renal cortex was 1,5 times higher than in renal medulla (p = 0,0001) and also higher than in total kidney (p = 0,001), in renal medulla it was lower than in total kidney (p = 0,002). In WKY rats, MARCKS mRNA expression level in renal cortex was higher than in renal medulla (p = 0,0005). There was no differences neither between renal cortex and total kidney (p = 0,011), nor between renal medulla and total kidney (p = 0,716). In SHR rats, NAP-22 mRNA expression level in renal cortex was twofold higher than in renal medulla (p = 0,001), in renal medulla it was lower than in total kidney (p = 0,005), the differences between renal cortex and total kidney were less significant (p = 0,011). In WKY rats, NAP-22 mRNA expression level in renal cortex was 1,5 times higher than in renal medulla (p = 0,001), while in renal medulla it was lower than in total kidney (p = 0,002). There was no significant difference in NAP-22 mRNA expression level between renal medulla and total kidney (p = 0,011). There were no significant interstrain differences in the animal groups either in the levels of MARCKS mRNA expression in renal cortex (p = 0,872), in renal medulla (p = 0,024) or in total kidney (p = 0,520). Neither there were differences in the levels of NAP-22 mRNA expression in cortex (p = 0,028), in medulla (p = 0,028) and in total kidney (p = 0,978).Conclusions. In both SHR and WKY rat strains, the level of MARCKS and NAP-22 mRNA expression in cortical and medullary kidney layers is different, in WKY rats these differences are less pronounced. At the same time, interstrain differences in NAP-22 and MARCKS mRNA expression levels in cortical, medullary layers and in total kidney of SHR and WKY rats were not found.
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Tanvetthayanont, Potsawat, Suppawiwat Ponglowhapan, Chutimon Thanaboonnipat, and Nan Choisunirachon. "Impact of gonadal status on ultrasonographic renal parenchymal dimensions in healthy cats." Journal of Feline Medicine and Surgery 22, no. 12 (March 20, 2020): 1148–54. http://dx.doi.org/10.1177/1098612x20910541.
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Objectives The aim of this study was to evaluate the effect of gonadal status on ultrasonographic renal parenchymal dimensions in healthy cats. Methods Forty healthy cats (10 intact males, 10 intact females, 10 castrated males and 10 spayed females) presented to the Division of Obstetrics, Gynecology and Reproduction, and the Diagnostic Imaging Unit at The Small Animal Teaching Hospital, Faculty of Veterinary Science, Chulalongkorn University. They were ultrasonographically examined to assess renal length, aortic luminal diameter, cortical thickness and medullary thickness. Results Regardless of gonadal status, the renal length, aortic luminal diameter, cortical thickness and medulla thickness of males were greater than those of females ( P <0.05). In general, neutered cats had thicker medullae (0.36 ± 0.08 cm) and higher mean renal length:aortic luminal diameter ratio (12.15 ± 1.48) than intact cats (0.32 ± 0.08 cm and 11.22 ± 1.37 cm, respectively) ( P <0.05), but no differences were observed in renal length, cortical thickness or aortic luminal diameter. Interestingly, when comparing between sexes with relatively equal body weight, only sex had an impact on renal length. Conclusions and relevance Gonadal status has an effect on medullary thickness and mean renal length:aortic luminal diameter ratio.
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Sureka, B., K. Bansal, and A. Arora. "Dense renal medulla sign." Indian Journal of Nephrology 26, no. 3 (2016): 223. http://dx.doi.org/10.4103/0971-4065.159554.
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Yuan, Baozhi, Mingyu Liang, Zhizhang Yang, Elizabeth Rute, Norman Taylor, Michael Olivier, and Allen W. Cowley. "Gene expression reveals vulnerability to oxidative stress and interstitial fibrosis of renal outer medulla to nonhypertensive elevations of ANG II." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 284, no. 5 (May 1, 2003): R1219—R1230. http://dx.doi.org/10.1152/ajpregu.00257.2002.
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The present study was designed to determine whether nonhypertensive elevations of plasma ANG II would modify the expression of genes involved in renal injury that could influence oxidative stress and extracellular matrix formation in the renal medulla using microarray, Northern, and Western blot techniques. Sprague-Dawley rats were infused intravenously with either ANG II (5 ng · kg−1 · min−1) or vehicle for 7 days ( n = 6/group). Mean arterial pressure averaged 110 ± 0.6 mmHg during the control period and 113 ± 0.4 mmHg after ANG II. The mRNA of 1,751 genes (∼80% of all currently known rat genes) that was differentially expressed (ANG II vs. saline) in renal outer and inner medulla was determined. The results of 12 hybridizations indicated that in response to ANG II, 11 genes were upregulated and 25 were downregulated in the outer medulla, while 11 were upregulated and 13 were downregulated in the inner medulla. These differentially expressed genes, most of which were not known previously to be affected by ANG II in the renal medulla, were found to group into eight physiological pathways known to influence renal injury and kidney function. Particularly, expression of several genes would be expected to increase oxidative stress and interstitial fibrosis in the outer medulla. Western blot analyses confirmed increased expression of transforming growth factor-β1 and collagen type IV proteins in the outer medulla. Results demonstrate that nonhypertensive elevations of plasma ANG II can significantly alter the expression of a variety of genes in the renal outer medulla and suggested the vulnerability of the renal outer medulla to the injurious effect of ANG II.
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Li, Ningjun, Fan Yi, Christina M. Sundy, Li Chen, Molly L. Hilliker, Dustin K. Donley, Daniel B. Muldoon, and Pin-Lan Li. "Expression and actions of HIF prolyl-4-hydroxylase in the rat kidneys." American Journal of Physiology-Renal Physiology 292, no. 1 (January 2007): F207—F216. http://dx.doi.org/10.1152/ajprenal.00457.2005.
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Hypoxia inducible factor (HIF) prolyl-4-hydroxylase domain-containing proteins (PHDs) promote the degradation of HIF-1α. Because HIF-1α is highly expressed in the renal medulla and HIF-1α-targeted genes such as nitric oxide synthase, cyclooxygenase, and heme oxygenase are important in the regulation of renal medullary function, we hypothesized that PHD regulates HIF-1α levels in the renal medulla and, thereby, participates in the control of renal Na+ excretion. Using real-time RT-PCR, Western blot, and immunohistochemical analyses, we have demonstrated that all three isoforms of PHD, PHD1, PHD2, and PHD3, are expressed in the kidneys and that PHD2 is the most abundant isoform. Regionally, all PHDs exhibited much higher levels in renal medulla than cortex. A furosemide-induced increase in renal medullary tissue Po2 significantly decreased PHD levels in renal medulla, whereas hypoxia significantly increased mRNA levels of PHDs in cultured renal medullary interstitial cells, indicating that O2 regulates PHDs. Functionally, the PHD inhibitor l-mimosine (l-Mim, 50 mg·kg−1·day−1 ip for 2 wk) substantially upregulated HIF-1α expression in the kidneys, especially in the renal medulla, and remarkably enhanced (by >80%) the natriuretic response to renal perfusion pressure in Sprague-Dawley rats. Inhibition of HIF transcriptional activity by renal medullary transfection of HIF-1α decoy oligodeoxynucleotides attenuated l-Mim-induced enhancement of pressure natriuresis, which confirmed that HIF-1α mediated the effect of l-Mim. These results indicate that highly expressed PHDs in the renal medulla make an important contribution to the control of renal Na+ excretion through regulation of HIF-1α and its targeted genes.
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Lee, Chang-Joon, Bruce S. Gardiner, Roger G. Evans, and David W. Smith. "Analysis of the critical determinants of renal medullary oxygenation." American Journal of Physiology-Renal Physiology 317, no. 6 (December 1, 2019): F1483—F1502. http://dx.doi.org/10.1152/ajprenal.00315.2019.
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We have previously developed a three-dimensional computational model of oxygen transport in the renal medulla. In the present study, we used this model to quantify the sensitivity of renal medullary oxygenation to four of its major known determinants: medullary blood flow (MBF), medullary oxygen consumption rate (V̇o2,M), hemoglobin (Hb) concentration in the blood, and renal perfusion pressure. We also examined medullary oxygenation under special conditions of hydropenia, extracellular fluid volume expansion by infusion of isotonic saline, and hemodilution during cardiopulmonary bypass. Under baseline (normal) conditions, the average medullary tissue Po2 predicted for the whole renal medulla was ~30 mmHg. The periphery of the interbundle region in the outer medulla was identified as the most hypoxic region in the renal medulla, which demonstrates that the model prediction is qualitatively accurate. Medullary oxygenation was most sensitive to changes in renal perfusion pressure followed by Hb, MBF, and V̇o2,M, in that order. The medullary oxygenation also became sensitized by prohypoxic changes in other parameters, leading to a greater fall in medullary tissue Po2 when multiple parameters changed simultaneously. Hydropenia did not induce a significant change in medullary oxygenation compared with the baseline state, while volume expansion resulted in a large increase in inner medulla tissue Po2 (by ~15 mmHg). Under conditions of cardiopulmonary bypass, the renal medulla became severely hypoxic, due to hemodilution, with one-third of the outer stripe of outer medulla tissue having a Po2 of <5 mmHg.
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Tharwat, Mohamed. "Ultrasonography of the Kidneys in Healthy and Diseased Camels (Camelus dromedarius)." Veterinary Medicine International 2020 (October 21, 2020): 1–12. http://dx.doi.org/10.1155/2020/7814927.
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This review article is written to describe the results of ultrasonography of the kidneys in healthy camels as well as camels with some renal disorders. In the dromedary camel, the physiology of the kidney is of interest in view of the specialization of the camel to hot dry deserts and to prolonged periods without water. It plays an important role in water conservation through the production of highly concentrated urine that may predispose animal to varieties of renal disorders. Examples of kidney affections in dromedary camels are renal capsular pigmentation, medullary hyperemia, subcapsular calcification, cortical and medullar discoloration, hemorrhage in renal pelvis, nephrolithiasis, and hydatidosis. Congestion, hemorrhage, hydronephrosis, acute glomerulonephritis, subacute glomerulonephritis, chronic glomerulonephritis, diffuse interstitial nephritis, focal interstitial nephritis, renal cyst, hyaline degeneration, renal amyloidosis, tubular nephrosis, pyelonephritis, hemosiderosis, and renal toxicity. When the kidney is examined by ultrasonography, the clinician can get sufficient information about the size, position, and echo patterns of the renal cortex and medulla and renal pelvis and outlines of the renal blood vessels. In recent years, ultrasonography has been used in camels for scanning of the healthy status as well as evaluation and determining the diagnosis and prognosis of diseased cases. Examples of diseases evaluated by ultrasonography are paratuberculosis, trypanosomiasis, pneumonia, pleurisy, gastrointestinal neoplasms, chronic peritonitis, splenic abscessation, and hepatic disorders. Of the renal disorders assessed by ultrasonography are nephrolithiasis, hydronephrosis, pyelonephritis, renal abscessation, and renal neoplasms. Ultrasound guidance in biopsy of renal specimens has also been reported in dromedary camels.
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Liu, Y., E. M. Tolbert, A. M. Sun, and L. D. Dworkin. "In vivo and in vitro evidence for increased expression of HGF receptor in kidney of diabetic rat." American Journal of Physiology-Renal Physiology 271, no. 6 (December 1, 1996): F1202—F1210. http://dx.doi.org/10.1152/ajprenal.1996.271.6.f1202.
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Renal hypertrophy develops early in the course of diabetes and has been linked to progressive renal disease. Although the mechanism of renal hypertrophy is unknown, evidence suggests that local alterations in the production of one or more growth factors and/or their receptors are crucial to this process. In this study, we demonstrate that the c-met protooncogene product, a tyrosine kinase receptor for hepatocyte growth factor (HGF), is increased in the kidney of the diabetic rat. Northern blot analysis showed that renal expression of the c-met gene was substantially increased in rats made diabetic by administration of streptozotocin. Immunohistochemical studies revealed that the protein for c-met was concordantly elevated in cortical and medullar tubular epithelium following the onset of diabetes. Moreover, in vitro studies demonstrated that short-term exposure to high glucose concentration markedly stimulated c-met expression in cultured proximal tubular (opossum kidney) and inner medulla collecting duct cells (mIMCD-3). The results of enhanced renal expression of c-met together with elevated HGF indicate that the HGF/c-met system is markedly activated in the diabetic rat. These findings suggest that the HGF/c-met system may play a role in the diabetic renal hypertrophy.
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Vizzard, M. A., A. Standish, and W. S. Ammons. "Renal afferent input to the ventrolateral medulla of the cat." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 263, no. 2 (August 1, 1992): R412—R422. http://dx.doi.org/10.1152/ajpregu.1992.263.2.r412.
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Experiments were performed to determine if information from the kidneys projects to the rostral ventrolateral medulla. Extracellular action potentials were recorded from 148 cells within the rostral ventrolateral medulla of alpha-chloralose-anesthetized cats. Cells within the rostral ventrolateral medulla were tested for responses to electrical stimulation of both left and right renal nerves. Electrical stimulation of renal nerves excited 144 cells (97.3%) and inhibited 4. The majority of cells received either bilateral or contralateral renal nerve input. Cells with bilateral renal nerve input responded to contralateral renal nerve stimulation with a significantly greater number of impulses compared with ipsilateral renal nerve stimulation (P less than 0.05). All cells but one responding to renal nerve stimulation had convergent somatic input. Comparisons between thresholds for cell responses and activation thresholds for the A and C volleys of the compound action potential recorded in the least splanchnic nerve revealed that 44 cells required activation of A delta-fibers, and 12 cells required activation of both A delta- and C-fibers. A conditioning stimulus applied to renal nerves on one side significantly decreased the response elicited by a test stimulus applied to the renal nerves on the opposite side for at least 300 ms (P less than 0.05). The demonstration that an afferent connection exists between the kidneys and the ventrolateral medulla suggests that the rostral ventrolateral medulla may play a role in mediating supraspinal reflexes of renal origin.
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Parivar, F., P. T. Narasimhan, and B. Ross. "Renal corticomedullary metabolite gradients during graded arterial occlusion: a localized 31P magnetic resonance spectroscopy study." Journal of the American Society of Nephrology 2, no. 2 (August 1991): 200–211. http://dx.doi.org/10.1681/asn.v22200.
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In order to investigate the role of the outer medulla in acute ischemic renal failure (Epstein FH, Balaban RS, Ross BD: Redox state of cytochrome aa3 in isolated perfused rat kidney. Am J Physiol 1982;243: F356-F363), the distribution of ATP in the in vivo porcine kidney and its relationship to Na transport and to ischemia was examined by using localized 31P magnetic resonance spectroscopy. Renal cortex (ATP) was higher than medulla. Reduction in Na transport produced by partial renal arterial occlusion ("hypofiltration"), resulted in a 13% increase in the ATP/Pi ratio of the whole kidney (from 2.61 +/- 0.26 to 2.96 +/- 0.27; P less than 0.03). This increase was accounted for by a statistically significant increase in (ATP) in the cortex, with medulla contributing to an insignificant extent. Further occlusion of the renal artery to reduce GFR to zero ("hypoperfusion") resulted in a 70% fall in ATP/Pi ratio. (ATP) was reduced most in the cortex, but pH fell equally in cortex and medulla. After release of arterial occlusion, cortical ATP recovered less completely than medulla ATP. Intracellular pH and Pi were restored in both cortex and medulla. It was concluded that cortex and medulla contribute equally to the pattern of disordered energy metabolism in acute renal failure. Sparing of ATP during hypofiltration may reflect the reduced energy requirements of active Na transport.
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Abdelkader, Amany, Julie Ho, Connie P. C. Ow, Gabriela A. Eppel, Niwanthi W. Rajapakse, Markus P. Schlaich, and Roger G. Evans. "Renal oxygenation in acute renal ischemia-reperfusion injury." American Journal of Physiology-Renal Physiology 306, no. 9 (May 1, 2014): F1026—F1038. http://dx.doi.org/10.1152/ajprenal.00281.2013.
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Tissue hypoxia has been demonstrated, in both the renal cortex and medulla, during the acute phase of reperfusion after ischemia induced by occlusion of the aorta upstream from the kidney. However, there are also recent clinical observations indicating relatively well preserved oxygenation in the nonfunctional transplanted kidney. To test whether severe acute kidney injury can occur in the absence of widespread renal tissue hypoxia, we measured cortical and inner medullary tissue Po2 as well as total renal O2 delivery (Do2) and O2 consumption (V̇o2) during the first 2 h of reperfusion after 60 min of occlusion of the renal artery in anesthetized rats. To perform this experiment, we used a new method for measuring kidney Do2 and V̇o2 that relies on implantation of fluorescence optodes in the femoral artery and renal vein. We were unable to detect reductions in renal cortical or inner medullary tissue Po2 during reperfusion after ischemia localized to the kidney. This is likely explained by the observation that V̇o2 (−57%) was reduced by at least as much as Do2 (−45%), due to a large reduction in glomerular filtration (−94%). However, localized tissue hypoxia, as evidence by pimonidazole adduct immunohistochemistry, was detected in kidneys subjected to ischemia and reperfusion, particularly in, but not exclusive to, the outer medulla. Thus, cellular hypoxia, particularly in the outer medulla, may still be present during reperfusion even when reductions in tissue Po2 are not detected in the cortex or inner medulla.
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Shi, Haikun, Daniel Patschan, Tracy Epstein, Michael S. Goligorsky, and Joseph Winaver. "Delayed recovery of renal regional blood flow in diabetic mice subjected to acute ischemic kidney injury." American Journal of Physiology-Renal Physiology 293, no. 5 (November 2007): F1512—F1517. http://dx.doi.org/10.1152/ajprenal.00215.2007.
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Ischemic acute kidney injury in experimental diabetes mellitus (DM) is associated with a more severe deterioration in renal function than shown in nondiabetic animals. We evaluated whether the early recovery phase from acute kidney injury is associated with a more prolonged and sustained decrease in renal perfusion in diabetic mice, which could contribute to the impaired recovery of renal function. Perfusion to the renal cortex and medulla was evaluated by laser-Doppler flowmetry in 10- to 12-wk-old anesthetized mice with type 2 DM ( db/db), heterozygous mice ( db/m), and nondiabetic (control) mice (C57BL/6J). After baseline measurements were obtained, the right renal artery was clampedfor 20 min followed by reperfusion for 60 min. The data demonstrated that, in all three groups studied, the reperfusion phase was characterized by a significant increase in the medullary-to-cortical blood flow ratio. Moreover, during recovery from ischemia, there was a marked prolongation in the time (in min) required to reach peak reperfusion in the cortex ( db/db: 20.7 ± 4.0, db/m: 12.92 ± 1.9, C57BL/6J: 9.3 ± 1.3) and the medulla ( db/db: 20.8 ± 3.2, db/m: 12.88 ± 1.89, C57BL/6J: 11.2 ± 1.2). Additionally, the slope of the recovery phase was lower in db/ db mice (cortex: 61.9 ± 23.1%/min, medulla: 16.3 ± 3.6%/min) than in C57BL/6J mice (cortex: 202.2 ± 41.6%/min, medulla: 42.1 ± 7.2%/min). Our findings indicate that renal ischemia is associated with a redistribution of blood flow from cortex to medulla, not related to DM. Furthermore, renal ischemia in db/db mice results in a marked impairment in reperfusion of the renal cortex and medulla during the early postischemic period.
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SMOYER, WILLIAM E., RICHARD RANSOM, RAYMOND C. HARRIS, MICHAEL J. WELSH, GUDRUN LUTSCH, and RAINER BENNDORF. "Ischemic Acute Renal Failure Induces Differential Expression of Small Heat Shock Proteins." Journal of the American Society of Nephrology 11, no. 2 (February 2000): 211–21. http://dx.doi.org/10.1681/asn.v112211.
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αB-crystallin and heat shock protein (hsp) 25 are structurally and functionally related small stress proteins induced by a variety of insults, including heat and ischemia. Cytoprotection by these two hsp is thought to result from molecular chaperoning and/or cytoskeletal stabilization. Because renal ischemia is characterized by disruption of the renal tubular cell actin cytoskeleton, this study was conducted to determine the localization and quantify the expression and phosphorylation of both hsp in renal cortex, isolated glomeruli, outer medulla, and inner medulla of rats after bilateral renal ischemia. Sham-operated kidneys had similarly small amounts of hsp25 and αB-crystallin in cortex and glomeruli, with substantially greater amounts of αB-crystallin versus hsp25 in outer and inner medulla. Ischemia resulted in significantly increased hsp25 (and hsp70i) but variable αB-crystallin levels in cortex and outer medulla, and progressively decreased glomerular hsp25 phosphorylation. In sham-operated kidneys, hsp25 localized to glomeruli, vessels, and collecting ducts, with αB-crystallin primarily in medullary thin limbs and collecting ducts. After ischemia, hsp25 accumulated in proximal tubules in cortex and outer medulla, while αB-crystallin labeling became nonhomogeneous in outer medulla, and increased in Bowman's capsule. It is concluded that: (1) There is striking differential expression of hsp25 and αB-crystallin in various renal compartments; and (2) Renal ischemia results in differential accumulation of hsp25 and αB-crystallin, with hsp25 part of a generalized stress response in renal proximal tubular cells, which may play a role in recovery from ischemia-induced actin filament disruption.
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Knepper, Mark A., Gerald M. Saidel, Vincent C. Hascall, and Terry Dwyer. "Concentration of solutes in the renal inner medulla: interstitial hyaluronan as a mechano-osmotic transducer." American Journal of Physiology-Renal Physiology 284, no. 3 (March 1, 2003): F433—F446. http://dx.doi.org/10.1152/ajprenal.00067.2002.
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Although the concentrating process in the renal outer medulla is well understood, the concentrating mechanism in the renal inner medulla remains an enigma. The purposes of this review are fourfold. 1) We summarize a theoretical basis for classifying all possible steady-state inner medullary countercurrent concentrating mechanisms based on mass balance principles. 2) We review the major hypotheses that have been proposed to explain the axial osmolality gradient in the interstitium of the renal inner medulla. 3) We summarize and expand on the Schmidt-Nielsen hypothesis that the contractions of the renal pelvocalyceal wall may provide an important energy source for concentration in the inner medulla. 4) We discuss the special properties of hyaluronan, a glycosaminoglycan that is the chief component of a gel-like renal inner medullary interstitial matrix, which may allow it to function as a mechano-osmotic transducer, converting energy from the contractions of the pelvic wall to an axial osmolality gradient in the medulla. These considerations set the stage for renewed experimental investigation of the urinary concentrating process and a new generation of mathematical models of the renal concentrating mechanism, which treat the inner medullary interstitium as a viscoelastic system rather than a purely hydraulic system.
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Gao, Yang, Melissa J. Romero-Aleshire, Qi Cai, Theodore J. Price, and Heddwen L. Brooks. "Rapamycin inhibition of mTORC1 reverses lithium-induced proliferation of renal collecting duct cells." American Journal of Physiology-Renal Physiology 305, no. 8 (October 15, 2013): F1201—F1208. http://dx.doi.org/10.1152/ajprenal.00153.2013.
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Nephrogenic diabetes insipidus (NDI) is the most common renal side effect in patients undergoing lithium therapy for bipolar affective disorders. Approximately 2 million US patients take lithium of whom ∼50% will have altered renal function and develop NDI ( 2 , 37 ). Lithium-induced NDI is a defect in the urinary concentrating mechanism. Lithium therapy also leads to proliferation and abundant renal cysts (microcysts), commonly in the collecting ducts of the cortico-medullary region. The mTOR pathway integrates nutrient and mitogen signals to control cell proliferation and cell growth (size) via the mTOR Complex 1 (mTORC1). To address our hypothesis that mTOR activation may be responsible for lithium-induced proliferation of collecting ducts, we fed mice lithium chronically and assessed mTORC1 signaling in the renal medulla. We demonstrate that mTOR signaling is activated in the renal collecting ducts of lithium-treated mice; lithium increased the phosphorylation of rS6 (Ser240/Ser244), p-TSC2 (Thr1462), and p-mTOR (Ser2448). Consistent with our hypothesis, treatment with rapamycin, an allosteric inhibitor of mTOR, reversed lithium-induced proliferation of medullary collecting duct cells and reduced levels of p-rS6 and p-mTOR. Medullary levels of p-GSK3β were increased in the renal medullas of lithium-treated mice and remained elevated following rapamycin treatment. However, mTOR inhibition did not improve lithium-induced NDI and did not restore the expression of collecting duct proteins aquaporin-2 or UT-A1.
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Zhu, Qing, Xiao-Xue Li, Weili Wang, Junping Hu, Pin-Lan Li, Sabena Conley, and Ningjun Li. "Mesenchymal stem cell transplantation inhibited high salt-induced activation of the NLRP3 inflammasome in the renal medulla in Dahl S rats." American Journal of Physiology-Renal Physiology 310, no. 7 (April 1, 2016): F621—F627. http://dx.doi.org/10.1152/ajprenal.00344.2015.
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Inflammasomes activate caspase-1 to produce interleukin (IL)-1β. Activation of the NLRP3 inflammasome is involved in various renal pathological conditions. It remains unknown whether the NLRP3 inflammasome activation participates in the abnormal renal response to high-salt (HS) diet in Dahl salt-sensitive (S) rats. In addition, our lab recently showed that transplantation of mesenchymal stem cells (MSCs) attenuated HS-induced inflammation in the renal medulla in Dahl S rat. However, it is unclear whether the anti-inflammatory action of MSCs is associated with inhibition of the NLRP3 inflammasome. The present study determined the response of the NLRP3 inflammasome to HS intake and the effect of MSC transplantation on the NLRP3 inflammasome in the renal medulla in Dahl S rats. Immunostaining showed that the inflammasome components NLRP3, ASC, and caspase-1 were mainly present in distal tubules and collecting ducts. Interestingly, the renal medullary levels of these inflammasome components were remarkably increased after a HS diet in Dahl S rats, while remaining unchanged in normal rats. This HS-induced activation of the NLRP3 inflammasome was significantly blocked by MSC transplantation into the renal medulla in Dahl S rats. Furthermore, infusion of a caspase-1 inhibitor into the renal medulla significantly attenuated HS-induced hypertension in Dahl S rats. These data suggest that HS-induced activation of the NLRP3 inflammasome may contribute to renal medullary dysfunction in Dahl S rats and that inhibition of inflammasome activation may be one of the mechanisms for the anti-inflammatory and anti-hypertensive effects of stem cells in the renal medulla in Dahl S rats.
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S., Thambidurai, Venkatesh Kasi Arunachalam, Rupa R., and Sriman R. "Role of Diffusion Tensor Imaging in Functional Assessment of Transplant Kidneys at 3-Tesla MRI." Journal of Gastrointestinal and Abdominal Radiology 3, S 01 (May 18, 2020): S7—S14. http://dx.doi.org/10.1055/s-0040-1709084.
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Abstract Objectives The main purpose of this article is to measure the fractional anisotropy (FA) and apparent diffusion coefficient (ADC) values of cortex and medulla of renal allograft using 3-Tesla diffusion tensor imaging (DTI) in renal transplant patients with normal and graft dysfunction and to assess the correlation between diffusion tensor parameters (ADC and FA) and the estimated glomerular filtration rate (eGFR) value. Materials and Methods Fifty renal transplant recipients who received either living or cadaveric renal allografts were included in the study. Blood samples for serum creatinine and eGFR value were taken on the same day prior to the magnetic resonance study and the patients were assigned to three groups (A, B, C) according to allograft function (eGFR levels). The mean ADC and FA values of the cortex/medulla in upper, mid, and lower poles were calculated from the DTI sequence. Statistical analysis was performed using paired sample Student’s t-test and one-way analysis of variance test. Results The mean ADC values of the cortex were higher than the medulla that was statistically significant. However, the mean FA values were significantly higher in the medulla than the cortex. Mean ADCs and FA of the renal cortex and medulla were significantly higher in group A patients with normal renal function than in group B and C with poor renal functions. The corticomedullary difference in the FA values was more in group A. However, this difference was lower in group B and more so in group C. Conclusion ADC and FA values in the renal cortex and medulla exhibit a good correlation with allograft function and were significantly lower in transplants with dysfunction than those with good function. FA values appear to be more sensitive than eGFR and ADC for detection of early pathological changes in the graft dysfunction.
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Cowley, Allen W., David L. Mattson, Shanhong Lu, and Richard J. Roman. "The Renal Medulla and Hypertension." Hypertension 25, no. 4 (April 1995): 663–73. http://dx.doi.org/10.1161/01.hyp.25.4.663.
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Beck, Franz-X., Adolf Dörge, and Klaus Thurau. "Cellular Osmoregulation in Renal Medulla." Kidney and Blood Pressure Research 11, no. 3-5 (1988): 174–86. http://dx.doi.org/10.1159/000173161.
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Kakoki, Masao, Hyung-Suk Kim, William J. Arendshorst, and David L. Mattson. "l-Arginine uptake affects nitric oxide production and blood flow in the renal medulla." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 287, no. 6 (December 2004): R1478—R1485. http://dx.doi.org/10.1152/ajpregu.00386.2004.
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Experiments were performed to determine whether l-arginine transport regulates nitric oxide (NO) production and hemodynamics in the renal medulla. The effects of renal medullary interstitial infusion of cationic amino acids, which compete with l-arginine for cellular uptake, on NO levels and blood flow in the medulla were examined in anesthetized rats. NO concentration in the renal inner medulla, measured with a microdialysis-oxyhemoglobin trapping technique, was significantly decreased by 26–44% and renal medullary blood flow, measured by laser Doppler flowmetry, was significantly reduced by 20–24% during the acute renal medullary interstitial infusion of l-ornithine, l-lysine, and l-homoarginine (1 μmol·kg−1·min−1 each; n = 6–8/group). In contrast, intramedullary infusion of l-arginine increased NO concentration and medullary blood flow. Flow cytometry experiments with 4-amino-5-methylamino-2′,7′-difluorescein diacetate, a fluorophore reactive to intracellular NO, demonstrated that l-ornithine, l-lysine, and l-homoarginine decreased NO by 54–57% of control, whereas l-arginine increased NO by 21% in freshly isolated inner medullary cells (1 mmol/l each, n > 1,000 cells/experiment). The mRNA for the cationic amino acid transporter-1 was predominantly expressed in the inner medulla, and cationic amino acid transporter-1 protein was localized by immunohistochemistry to the collecting ducts and vasa recta in the inner medulla. These results suggest that l-arginine transport by cationic amino acid transport mechanisms is important in the production of NO and maintenance of blood flow in the renal medulla.
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Rashwan, Ahmed, and Sahar Mahmoud. "Localization of Different Lectins and E-cadherin in the kidney of a Balady Egyptian Duck." Alexandria Journal of Veterinary Sciences 75, no. 1 (2022): 1. http://dx.doi.org/10.5455/ajvs.124612.
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The purpose of our present study is to determine the spatial pattern of different lectins and E-cadherin in the duck kidney, which has never been done before. We checked the localization of six different lectins in the adult duck kidney of both sexes by histochemistry using wheat germ agglutinin (WGA), ricinus communis agglutinin (RCA), peanut agglutinin (PNA), dolichos Biflorus Agglutinin (DBA), concanavalin (Con A) and griffonia simplicifolia agglutinin-I (GSA-I). We found different locations of lectins in the duck nephron and this difference may be related to the function of each lectin. WGA lectin had intense reactions in the proximal and distal convoluted tubules (PCT and DCT) but was not present in the renal corpuscle of the renal cortex. WGA was also intense in the medulla especially in the collecting ducts (CD) and collecting tubules (CT). RCA was intense in the renal corpuscle, moderate in in the renal cortex tubules, and intense in the medulla tubules. PNA was moderate in the tubules of renal cortex and renal corpuscle while in the medulla, PNA had intense reaction. Con A, GSA-I and DBA lectins had mild to moderate reactions in the renal cortex and also in the medulla. Con A and GSA-I had intense reactions in the renal corpuscles. E-cadherin, which is responsible for maintaining cell polarity, was located in the lateral epithelial cells of all tubes and ducts in the renal cortex and medulla and not present in the renal corpuscle. There are no previous studies describing the location of different lectins and E-cadherin in duck kidneys. Our study clarifies the distribution pattern of various lectins and E-cadherin, which may be useful for comprehending how these lectins and E-cadherin work in the duck kidney.
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Curtis, Lisa M., Sifeng Chen, Bo Chen, Anupam Agarwal, Christopher A. Klug, and Paul W. Sanders. "Contribution of intrarenal cells to cellular repair after acute kidney injury: subcapsular implantation technique." American Journal of Physiology-Renal Physiology 295, no. 1 (July 2008): F310—F314. http://dx.doi.org/10.1152/ajprenal.90205.2008.
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The kidney is capable of regeneration following injury, particularly following acute insults. Although the mechanisms underlying cellular regeneration are incompletely understood, emerging evidence suggests a role for cells of renal origin in the repair and replacement of damaged renal tubule cells. The overall hypothesis of this study is that native kidney cells that reside in a niche in the kidney provide robust contribution to the repair of kidney tubules following injury. To test this hypothesis, we utilized a model of renal ischemia-reperfusion injury that results in extensive morphological changes, particularly in the outer medulla. Renal tissue obtained from mice constitutively expressing Escherichia coli β-galactosidase (ROSA26) was dissected from the cortex, outer medulla, or papilla and implanted under the renal capsule of the injured mice. Mice were allowed to recover for 7 days. Sections through the injured kidney demonstrated the presence of implant-derived cells in renal tubules in the outer medulla. The implanted renal region that exhibited the most robust response was the papilla, whereas tissue pieces from the cortex and outer medulla showed less contribution to recipient renal tubules. These results provide proof-of-principle evidence that renal-derived reparative cells reside in all regions of the kidney, perhaps more predominantly in the renal papilla. A greater understanding of the cell biology of renal repair by native kidney cells will provide further insight into the design of novel therapies in acute kidney injury, and the subcapsular implant technique described in this study may offer unique advantages to evaluate renal repair mechanisms.
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Nishiyama, Akira, Shoji Kimura, Toshiki Fukui, Matlubur Rahman, Hirohito Yoneyama, Hiroaki Kosaka, and Youichi Abe. "Blood flow-dependent changes in renal interstitial guanosine 3′,5′-cyclic monophosphate in rabbits." American Journal of Physiology-Renal Physiology 282, no. 2 (February 1, 2002): F238—F244. http://dx.doi.org/10.1152/ajprenal.00087.2001.
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We examined responses of renal interstitial guanosine 3′,5′-cyclic monophosphate (cGMP) to changes in renal perfusion pressure (RPP) within and below the range of renal blood flow (RBF) autoregulation. A microdialysis method was used to monitor renal cortical and medullary interstitial cGMP levels in anesthetized rabbits. RPP was reduced in two steps: from ambient pressure (89 ± 3 mmHg) to 70 ± 2 mmHg ( step 1) and then to 48 ± 3 mmHg ( step 2). RBF was maintained in step 1 but was significantly decreased in step 2 from 2.94 ± 0.23 to 1.47 ± 0.08 ml · min−1 · g−1. Basal interstitial concentrations of cGMP were significantly lower in the cortex than in the medulla (12.1 ± 1.4 and 19.9 ± 0.4 nmol/l, respectively). Cortical and medullary cGMP did not change in step 1 but were significantly decreased in step 2, with significantly less reduction in cGMP concentrations in the medulla than in the cortex (−25 ± 3 and −44 ± 3%, respectively). Over this pressure range, changes in cortical and medullary cGMP were highly correlated with changes in RBF ( r= 0.94, P < 0.005 for cortex; r = 0.82, P < 0.01 for medulla). Renal interstitial nitrate/nitrite was not changed in step 1 but was significantly decreased in step 2 (−38 ± 2% in cortex and −20 ± 2% in medulla). Nitric oxide synthase inhibition with N G-nitro-l-arginine methyl ester (l-NAME, 30 mg/kg bolus, 50 mg · kg−1 · h−1 iv infusion) significantly decreased RBF (by −46 ± 4%) and interstitial concentrations of cGMP (−27 ± 4% in cortex and −22 ± 4% in medulla, respectively). During l-NAME treatment, renal interstitial concentrations of cGMP in the cortex and medulla were similarly not altered in step 1. However, l-NAME significantly attenuated cGMP responses to a reduction in RPP in step 2. These results indicate that acute changes in RBF result in alterations in nitric oxide-dependent renal interstitial cGMP levels, with differential effects in the medulla compared with the cortex.
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Cowley, Allen W., Takefumi Mori, David Mattson, and Ai-Ping Zou. "Role of renal NO production in the regulation of medullary blood flow." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 284, no. 6 (June 1, 2003): R1355—R1369. http://dx.doi.org/10.1152/ajpregu.00701.2002.
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The unique role of nitric oxide (NO) in the regulation of renal medullary function is supported by the evidence summarized in this review. The impact of reduced production of NO within the renal medulla on the delivery of blood to the medulla and on the long-term regulation of sodium excretion and blood pressure is described. It is evident that medullary NO production serves as an important counterregulatory factor to buffer vasoconstrictor hormone-induced reduction of medullary blood flow and tissue oxygen levels. When NO synthase (NOS) activity is reduced within the renal medulla, either pharmacologically or genetically [Dahl salt-sensitive (S) rats], a super sensitivity to vasoconstrictors develops with ensuing hypertension. Reduced NO production may also result from reduced cellular uptake of l-arginine in the medullary tissue, resulting in hypertension. It is concluded that NO production in the renal medulla plays a very important role in sodium and water homeostasis and the long-term control of arterial pressure.
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Layton, Anita T., Thomas L. Pannabecker, William H. Dantzler, and Harold E. Layton. "Hyperfiltration and inner stripe hypertrophy may explain findings by Gamble and coworkers." American Journal of Physiology-Renal Physiology 298, no. 4 (April 2010): F962—F972. http://dx.doi.org/10.1152/ajprenal.00250.2009.
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Simulations conducted in a mathematical model were used to exemplify the hypothesis that elevated solute concentrations and tubular flows at the boundary of the renal outer and inner medullas of rats may contribute to increased urine osmolalities and urine flow rates. Such elevated quantities at that boundary may arise from hyperfiltration and from inner stripe hypertrophy, which are correlated with increased concentrating activity (Bankir L, Kriz W. Kidney Int. 47: 7–24, 1995). The simulations used the region-based model for the rat inner medulla that was presented in the companion study (Layton AT, Pannabecker TL, Dantzler WH, Layton HE. Am J Physiol Renal Physiol 298: F000–F000, 2010). The simulations were suggested by experiments which were conducted in rat by Gamble et al. (Gamble JL, McKhann CF, Butler AM, Tuthill E. Am J Physiol 109: 139–154, 1934) in which the ratio of NaCl to urea in the diet was systematically varied in eight successive 5-day intervals. The simulations predict that changes in boundary conditions at the boundary of the outer and inner medulla, accompanied by plausible modifications in transport properties of the collecting duct system, can significantly increase urine osmolality and flow rate. This hyperfiltration-hypertrophy hypothesis may explain the finding by Gamble et al. that the maximum urine osmolality attained from supplemental feeding of urea and NaCl in the eight intervals depends on NaCl being the initial predominant solute and on urea being the final predominant solute, because urea in sufficient quantity appears to stimulate concentrating activity. More generally, the hypothesis suggests that high osmolalities and urine flow rates may depend, in large part, on adaptive modifications of cortical hemodynamics and on outer medullary structure and not entirely on an extraordinary concentrating capability that is intrinsic to the inner medulla.
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Brown, J., S. P. Salas, and J. M. Polak. "Renal atrial natriuretic peptide receptor subtypes in spontaneously hypertensive rats." American Journal of Physiology-Renal Physiology 259, no. 4 (October 1, 1990): F605—F612. http://dx.doi.org/10.1152/ajprenal.1990.259.4.f605.
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Receptor subtypes for atrial natriuretic peptide (ANP) were characterized in kidneys of 18-wk-old Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR) by in vitro autoradiography through use of des[Gln18, Ser19, Gly20, Leu21, Gly22] ANP-(4–23) (C-ANP) and ANP-(5–25) as subtype-selective ligands. alpha-125I-ANP (100 pM) bound reversibly but with high affinity to glomeruli, to stripes in outer medulla, and to inner medulla of both WKY and SHR. C-ANP (10 microM) inhibited approximately 70% of the glomerular binding but none of the medullary binding in either strain. All high-affinity specifically reversible binding sites for alpha-ANP that bound C-ANP were also bound by 10 microM ANP-(5–25). However, the specifically reversible binding of alpha-125I-ANP that was not inhibited by 10 microM C-ANP behaved differently in each strain. In WKY, this binding was weakly inhibited by ANP-(5–25), so that even the presence of 10 microM ANP-(5–25) did not inhibit some glomerular binding and greater than 40% of the specifically reversible medullary binding of alpha-125I-ANP. In SHR, this binding was inhibited by ANP-(5–25) with a significantly higher affinity so that all specifically reversible binding of alpha-125I-ANP was inhibited by 10 microM ANP-(5–25). SHR also showed higher affinities but lower maximum binding capacities for alpha-ANP in their outer cortical glomeruli and medullas. These results suggest that the preponderant medullary ANP receptor differs between WKY and SHR. Differences in glomerular subtypes of ANP receptor may also distinguish WKY and SHR.
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Kwon, Min Seong, Sun Woo Lim, and H. Moo Kwon. "Hypertonic Stress in the Kidney: A Necessary Evil." Physiology 24, no. 3 (June 2009): 186–91. http://dx.doi.org/10.1152/physiol.00005.2009.
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The interstitium of the renal medulla is hypertonic, imposing deleterious effects on local cells. At the same time, the hypertonicity provides osmotic gradient for water reabsorption and is a local signal for tissue-specific gene expression and differentiation of the renal medulla, which is a critical organ for water homeostasis.
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Liu, Yupin P., Rui Song, Chang hong Liang, Xin Chen, and Bo Liu. "Arterial spin labeling blood flow magnetic resonance imaging for evaluation of renal injury." American Journal of Physiology-Renal Physiology 303, no. 4 (August 15, 2012): F551—F558. http://dx.doi.org/10.1152/ajprenal.00288.2011.
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A multitude of evidence suggests that iodinated contrast material causes nephrotoxicity; however, there have been no previous studies that use arterial spin labeling (ASL) blood flow functional magnetic resonance imaging (fMRI) to investigate the alterations in effective renal plasma flow between normointensive and hypertensive rats following injection of contrast media. We hypothesized that FAIR-SSFSE arterial spin labeling MRI may enable noninvasive and quantitative assessment of regional renal blood flow abnormalities and correlate with disease severity as assessed by histological methods. Renal blood flow (RBF) values of the cortex and medulla of rat kidneys were obtained from ASL images postprocessed at ADW4.3 workstation 0.3, 24, 48, and 72 h before and after injection of iodinated contrast media (6 ml/kg). The H&E method for morphometric measurements was used to confirm the MRI findings. The RBF values of the outer medulla were lower than those of the cortex and the inner medulla as reported previously. Iodinated contrast media treatment resulted in decreases in RBF in the outer medulla and cortex in spontaneously hypertensive rats (SHR), but only in the outer medulla in normotensive rats. The iodinated contrast agent significantly decreased the RBF value in the outer medulla and the cortex in SHR compared with normotensive rats after injection of the iodinated contrast media. Histological observations of kidney morphology were also consistent with ASL perfusion changes. These results demonstrate that the RBF value can reflect changes of renal perfusion in the cortex and medulla. ASL-MRI is a feasible and accurate method for evaluating nephrotoxic drugs-induced kidney damage.
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Kakoki, Masao, Ai-Ping Zou, and David L. Mattson. "The influence of nitric oxide synthase 1 on blood flow and interstitial nitric oxide in the kidney." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 281, no. 1 (July 1, 2001): R91—R97. http://dx.doi.org/10.1152/ajpregu.2001.281.1.r91.
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The role of nitric oxide (NO) produced by NO synthase 1 (NOS1) in the renal vasculature remains undetermined. In the present study, we investigated the influence of systemic inhibition of NOS1 by intravenous administration of N ω-propyl-l-arginine (l-NPA; 1 mg · kg−1 · h−1) and N 5-(1-imino-3-butenyl)-l-ornithine (v-NIO; 1 mg · kg−1 · h−1), highly selective NOS1 inhibitors, on renal cortical and medullary blood flow and interstitial NO concentration in Sprague-Dawley rats. Arterial blood pressure was significantly decreased by administration of both NOS1-selective inhibitors (−11 ± 1 mmHg with l-NPA and −7 ± 1 mmHg with v-NIO; n = 9/group). Laser-Doppler flowmetry experiments demonstrated that blood flow in the renal cortex and medulla was not significantly altered following administration of either NOS1-selective inhibitor. In contrast, the renal interstitial level of NO assessed by an in vivo microdialysis oxyhemoglobin-trapping technique was significantly decreased in both the renal cortex (by 36–42%) and medulla (by 32–40%) following administration of l-NPA ( n = 8) or v-NIO ( n = 8). Subsequent infusion of the nonspecific NOS inhibitor N ω-nitro-l-arginine methyl ester (l-NAME; 50 mg · kg−1 · h−1) to rats pretreated with either of the NOS1-selective inhibitors significantly increased mean arterial pressure by 38–45 mmHg and significantly decreased cortical (25–29%) and medullary (37–43%) blood flow. In addition, l-NAME further decreased NO in the renal cortex (73–77%) and medulla (62–71%). To determine if a 40% decrease in NO could alter renal blood flow, a lower dose ofl-NAME (5 mg · kg−1 · h−1; n = 8) was administered to a separate group of rats. The low dose of l-NAME reduced interstitial NO (cortex 39%, medulla 38%) and significantly decreased blood flow (cortex 23–24%, medulla 31–33%). These results suggest that NOS1 does not regulate basal blood flow in the renal cortex or medulla, despite the observation that a considerable portion of NO in the renal interstitial space appears to be produced by NOS1.
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Chow, L. H., S. Subramanian, G. J. Nuovo, F. Miller, and E. P. Nord. "Endothelin receptor mRNA expression in renal medulla identified by in situ RT-PCR." American Journal of Physiology-Renal Physiology 269, no. 3 (September 1, 1995): F449—F457. http://dx.doi.org/10.1152/ajprenal.1995.269.3.f449.
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Three subtypes of endothelin (ET) receptors have been identified by cDNA cloning, namely ET-RA, ET-RB, and ET-RC. In the current study the precise cellular distribution of the ET receptor subtypes in the renal medulla was explored by detecting the corresponding polymerase chain reaction (PCR)-amplified cDNAs by in situ reverse transcription (RT)-PCR. The PCR-amplified cDNAs were detected either by direct incorporation using digoxigenin-dUTP (dig-dUTP) as a nucleotide substrate in the PCR reaction or by in situ hybridization with the dig-dUTP-labeled probe. ET-RB mRNA was detected exclusively in the epithelial cells of the inner and outer medullary collecting duct. In contrast, ET-RA message was observed primarily in interstitial cells and pericytes of the vasae rectae in the outer and inner medulla. Southern blot analysis of PCR-amplified cDNAs reverse transcribed from extracted RNA of rat renal medulla confirmed the specificity of the RT-PCR products. ET-RC mRNA was not detected. We conclude that ET-RB is the major ET receptor found in rat renal medulla and is expressed exclusively on inner medullary collecting duct cells. The pattern of ET receptor mRNA expression described suggests different physiological actions for ET on the diverse cellular structures of the renal medulla.
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Han, J. S., K. A. Thompson, C. L. Chou, and M. A. Knepper. "Experimental tests of three-dimensional model of urinary concentrating mechanism." Journal of the American Society of Nephrology 2, no. 12 (June 1992): 1677–88. http://dx.doi.org/10.1681/asn.v2121677.
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Recently, a new model of the urinary concentrating process has been proposed that takes into account the three-dimensional architecture of the renal medulla. Under the assumptions of the model, computer simulations predicted significant axial osmolality gradients in the inner medulla without active transport by the inner medullary loop of Henle. Two of the model assumptions (which constitute hypotheses for this study) were: (1) the osmotic water permeability of the initial part of the inner medullary collecting duct (initial IMCD) is very low even in the presence of vasopressin; and (2) there is significant lateral separation of structures such that thin descending limbs are far from the collecting ducts at the same inner medullary level. The first hypothesis was addressed by perfusing rat initial IMCD segments in vitro and measuring osmotic water permeability. With the osmotic gradient oriented as predicted by the model (lumen greater than bath), vasopressin increased the osmotic water permeability from 286 to 852 microns/s. Three additional series of experiments confirmed the high water permeability in the presence of vasopressin. The second hypothesis was addressed by morphometric analysis of histologic cross-sections of the rat renal medulla. Mean distances of descending limbs to the nearest adjacent collecting duct were very small throughout the inner medulla (less than 6 microns) and substantially less than in the outer medulla (28 microns). It was concluded that the data are inconsistent with both hypotheses and therefore do not support the feasibility of the "three-dimensional" model of the renal inner medulla. The axial distributions of loops of Henle and collecting ducts in the rat renal medulla are also reported.
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Stephenson, G., and J. Funder. "Hippocampal and renal type I receptors are differentially regulated." American Journal of Physiology-Endocrinology and Metabolism 252, no. 4 (April 1, 1987): E525—E529. http://dx.doi.org/10.1152/ajpendo.1987.252.4.e525.
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Previously, we have shown that renal mineralocorticoid receptors and hippocampal "corticosterone-perferring" sites have identical intrinsic steroid specificity in vitro. Others have shown that the aldosterone binding species in kidney and hippocampus have identical trypsin fragmentation patterns on isoelectric focusing. To further explore possible areas of identity, we determined levels of type I receptors in hippocampus, renal outer medulla cortex, and renal inner medulla papilla from 22 min to 16 days after adrenalectomy. Available type I sites in kidney fractions increased postadrenalectomy to plateau levels in 22 (inner medulla papilla) or 90 min (outer medulla cortex). In contrast, available hippocampal receptors attained maximal levels 24-48 h postadrenalectomy. Animals, 24-h adrenalectomized, showed no differences in steroid uptake or washout between kidney and hippocampus, determined by in vitro tracer binding 22 or 90 min after intravenous aldosterone or corticosterone. We interpret the marked difference in receptor levels between kidney and hippocampus postadrenalectomy as evidence for tissue-specific differences in the control of receptor levels by endogenous steroids.
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Kaneko, T., M. Takenaka, M. Okabe, Y. Yoshimura, A. Yamauchi, M. Horio, H. M. Kwon, J. S. Handler, and E. Imai. "Osmolarity in renal medulla of transgenic mice regulates transcription via 5'-flanking region of canine BGT1 gene." American Journal of Physiology-Renal Physiology 272, no. 5 (May 1, 1997): F610—F616. http://dx.doi.org/10.1152/ajprenal.1997.272.5.f610.
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Betaine is a major compatible osmolyte accumulated in the mammalian kidney medulla and in Madin-Darby canine kidney cells in response to hypertonicity. The accumulation is the result of an increase in maximal velocity of the Na(+)- and Cl-coupled betaine transporter designated BGT1. We have previously cloned the canine BGT1 gene and identified a tonicity-responsive enhancer element (TonE) in its 5'-flanking region. Here we report studies of transgenic mice that have in their genome 2.4 kb of the 5'-flanking region of the canine BGT1 gene in front of a chloramphenicol acetyl-transferase (CAT) reporter. Expression of CAT mRNA was detected only in the renal medulla and was increased by experimental manipulations that increase the tonicity of the renal medulla and decreased by manipulations that decrease medullary tonicity. We conclude that the 2.4-kb 5'-flanking region of the BGT1 gene mediates an increase in transcription in response to hyperosmolarity in the renal medulla.
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ZOU, AI-PING, ZHI-ZHANG YANG, PIN-LAN LI, and ALLEN W. COWLEY. "Oxygen-dependent expression of hypoxia-inducible factor-1α in renal medullary cells of rats." Physiological Genomics 6, no. 3 (August 28, 2001): 159–68. http://dx.doi.org/10.1152/physiolgenomics.2001.6.3.159.
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Hypoxia-inducible factor-1α (HIF-1α) is a transcription factor that regulates the oxygen-dependent expression of a number of genes. This transcription factor may contribute to the abundant expression of many genes in renal medullary cells that function normally under hypoxic conditions. The present study was designed to determine the characteristics of HIF-1α cDNA cloned from the rat kidney and the expression profile of HIF-1α in different kidney regions and to explore the mechanism activating or regulating HIF-1α expression in renal medullary cells. A 3,718-bp HIF-1α cDNA from the rat kidney was first cloned and sequenced using RT-PCR and TA cloning technique. It was found that 823 amino acids deduced from this renal HIF-1α cDNA had 99%, 96%, and 90% identity with rat, mouse, or human HIF-1α deposited in GenBank, respectively. The 3′-untranslated region of HIF-1α mRNA from the rat kidney contained seven AUUUA instability elements, five of which were found to be conserved among rat, mouse, and human HIF-1α. Northern blot analyses demonstrated a corticomedullary gradient of HIF-1α mRNA expression in the kidney, with the greatest abundance in the renal inner medulla. Western blot analyses also detected a higher HIF-1α protein level in the nuclear extracts from the renal medulla than the renal cortex. A classic loop diuretic, furosemide (10 mg/kg ip), markedly increased renal medullary Po2 levels from 22.5 to 52.2 mmHg, which was accompanied by a significant reduction of HIF-1α transcripts in renal medullary tissue. In in vitro experiments, low Po2, but not elevated osmolarity, was found to significantly increase HIF-1α mRNA in renal medullary interstitial cells and inner medullary collecting duct cells. These results indicate that HIF-1α is more abundantly expressed in the renal medulla compared with the renal cortex. Increased abundance of HIF-1α mRNA in the renal medulla may represent an adaptive response of renal medullary cells to low Po2.
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McLarnon, Sarah R., Katie Wilson, Bansari Patel, Jingping Sun, Christina L. Sartain, Christopher D. Mejias, Jacqueline B. Musall, et al. "Lipopolysaccharide Pretreatment Prevents Medullary Vascular Congestion following Renal Ischemia by Limiting Early Reperfusion of the Medullary Circulation." Journal of the American Society of Nephrology 33, no. 4 (February 3, 2022): 769–85. http://dx.doi.org/10.1681/asn.2021081089.
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BackgroundVascular congestion of the renal medulla—trapped red blood cells in the medullary microvasculature—is a hallmark finding at autopsy in patients with ischemic acute tubular necrosis. Despite this, the pathogenesis of vascular congestion is not well defined.MethodsIn this study, to investigate the pathogenesis of vascular congestion and its role in promoting renal injury, we assessed renal vascular congestion and tubular injury after ischemia reperfusion in rats pretreated with low-dose LPS or saline (control). We used laser Doppler flowmetry to determine whether pretreatment with low-dose LPS prevented vascular congestion by altering renal hemodynamics during reperfusion.ResultsWe found that vascular congestion originated during the ischemic period in the renal venous circulation. In control animals, the return of blood flow was followed by the development of congestion in the capillary plexus of the outer medulla and severe tubular injury early in reperfusion. Laser Doppler flowmetry indicated that blood flow returned rapidly to the medulla, several minutes before recovery of full cortical perfusion. In contrast, LPS pretreatment prevented both the formation of medullary congestion and its associated tubular injury. Laser Doppler flowmetry in LPS-pretreated rats suggested that limiting early reperfusion of the medulla facilitated this protective effect, because it allowed cortical perfusion to recover and clear congestion from the large cortical veins, which also drain the medulla.ConclusionsBlockage of the renal venous vessels and a mismatch in the timing of cortical and medullary reperfusion results in congestion of the outer medulla’s capillary plexus and promotes early tubular injury after renal ischemia. These findings indicate that hemodynamics during reperfusion contribute to the renal medulla’s susceptibility to ischemic injury.
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Lee, Sang Do, Soo Youn Choi, and H. Moo Kwon. "Distinct cellular pathways for resistance to urea stress and hypertonic stress." American Journal of Physiology-Cell Physiology 300, no. 3 (March 2011): C692—C696. http://dx.doi.org/10.1152/ajpcell.00150.2010.
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During antidiuresis with elevated vasopressin, urea accumulates in the renal medulla to very high concentrations, imposing considerable cellular stress. How local cells cope with urea stress is relevant to the whole kidney because the renal medulla is the major site of residence for the renal stem cells. Previous studies showed that renal cells were incapable of preconditioning in moderate urea concentrations to enhance resistance to urea stress. Instead, preconditioning in moderately high salinity (moderate hypertonicity) has been shown to promote resistance to urea stress due to the induction of the molecular chaperone heat shock protein 70 (Hsp70), which is mediated by the transcription factor tonicity-responsive enhancer binding protein (TonEBP). Here we report that cell lines derived from the kidney and fibroblasts display enhanced resistance to urea stress after pretreatment in moderate, nonstressful concentrations of urea. Using TonEBP knockdown and immunoblot analyses, we demonstrate that TonEBP and Hsp70 are dispensable for the increased resistance to urea stress. These data suggest that cells in the renal medulla are capable of overcoming urea stress by activating distinct cellular pathways.
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Zimmerhackl, B., C. R. Robertson, and R. L. Jamison. "The microcirculation of the renal medulla." Circulation Research 57, no. 5 (November 1985): 657–67. http://dx.doi.org/10.1161/01.res.57.5.657.
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Marais, James. "Microvasculature of the Feline Renal Medulla." Cells Tissues Organs 133, no. 1 (1988): 86–88. http://dx.doi.org/10.1159/000146620.
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Cowley, A. W., and R. R. Roman. "Countercurrent exchange in the renal medulla." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 284, no. 5 (May 1, 2003): R1151. http://dx.doi.org/10.1152/ajpregu.00064.2003.
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Pallone, Thomas L., Malcolm R. Turner, Aurélie Edwards, and Rex L. Jamison. "Countercurrent exchange in the renal medulla." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 284, no. 5 (May 1, 2003): R1153—R1175. http://dx.doi.org/10.1152/ajpregu.00657.2002.
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The microcirculation of the renal medulla traps NaCl and urea deposited to the interstitium by the loops of Henle and collecting ducts. Theories have predicted that countercurrent exchanger efficiency is favored by high permeability to solute. In contrast to the conceptualization of vasa recta as simple “U-tube” diffusive exchangers, many findings have revealed surprising complexity. Tubular-vascular relationships in the outer and inner medulla differ markedly. The wall structure and transport properties of descending vasa recta (DVR) and ascending vasa recta (AVR) are very different. The recent discoveries of aquaporin-1 (AQP1) water channels and the facilitated urea carrier UTB in DVR endothelia show that transcellular as well as paracellular pathways are involved in equilibration of DVR plasma with the interstitium. Efflux of water across AQP1 excludes NaCl and urea, leading to the conclusion that both water abstraction and diffusion contribute to transmural equilibration. Recent theory predicts that loss of water from DVR to the interstitium favors optimization of urinary concentration by shunting water to AVR, secondarily lowering blood flow to the inner medulla. Finally, DVR are vasoactive, arteriolar microvessels that are anatomically positioned to regulate total and regional blood flow to the outer and inner medulla. In this review, we provide historical perspective, describe the current state of knowledge, and suggest areas that are in need of further exploration.
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Yu, Jing. "Wnt signaling and renal medulla formation." Pediatric Nephrology 26, no. 9 (September 2011): 1553–57. http://dx.doi.org/10.1007/s00467-011-1888-8.
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Pedersen, Michael, Zsolt Vajda, Hans Stødkilde-Jørgensen, Søren Nielsen, and Jørgen Frøkiær. "Furosemide increases water content in renal tissue." American Journal of Physiology-Renal Physiology 292, no. 5 (May 2007): F1645—F1651. http://dx.doi.org/10.1152/ajprenal.00060.2006.
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The present study was designed to evaluate the short-term effects of intravenous administration of furosemide on key functions in the kidney cortex and the outer and inner medulla of rats by using magnetic resonance imaging (MRI). Renal tissue water content, renal tissue oxygenation (in relation to the magnetic resonance spin-spin relaxation rate), the apparent diffusion coefficient (ADC) of water, and volume of renal blood flow were measured. Furosemide administration resulted in an increased water content in all regions of the kidney. In parallel with this, we found a significant reduction in ADC in the cortex (2.7 ± 0.1 × 10−3 to 2.3 ± 0.1 × 10−3 mm2/s; P < 0.01) and in the outer medulla (2.3 ± 0.1 × 10−3 to 2.0 ± 0.1 × 10−3 mm2/s; P < 0.01), indicating that the intra- to extracellular volume fraction of water increased in response to furosemide administration. Furosemide also decreased the blood oxygenation in the cortex (49.1 ± 2.9 to 40.9 ± 2.0 s−1; P < 0.01), outer medulla (41.9 ± 2.8 to 33.2 ± 1.6 s−1; P < 0.01) and in the inner medulla (37.1 ± 2.9 to 26.7 ± 1.8 s−1; P < 0.01), indicating an increased amount of oxygenated Hb in the renal tissue. Moreover, renal blood flow decreased in response to furosemide (6.9 ± 0.2 to 4.4 ± 0.2 ml/min; P < 0.001). In conclusion, furosemide administration was associated with increased renal water content, an increase in the intra- to extracellular volume fraction of water, an increased oxygen tension, and a decrease in the renal blood flow. Thus MRI provides an integrated evaluation of changes in renal function, leading to decreased renal water and solute reabsorption in response to furosemide, and, in addition, MRI provides an alternative tool to monitor noninvasively changes at the cellular level.