The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
MeSH Review

Loop of Henle

Welcome! If you are familiar with the subject of this article, you can contribute to this open access knowledge base by deleting incorrect information, restructuring or completely rewriting any text. Read more.

Disease relevance of Loop of Henle

  • The main pathogenic factors of the impaired water excretion in human cirrhosis are an increased plasma concentration of AVP, a reduced renal synthesis of prostaglandins and a reduced delivery of filtrate to the ascending limb of the loop of Henle [1].
  • The demonstrated alteration in nephron function during relapse of nephrotic syndrome could result from either (1) a decrease in the amount of sodium delivered to the ascending limb of the loop of Henle because of increased proximal reabsorption or (2) a change in the intrinsic characteristics for sodium reabsorption in that segment [2].
  • OBJECTIVE: To assess the prevalence of thiamin deficiency in patients with congestive heart failure who are treated with diuretics that inhibit sodium and chloride reabsorption in the thick ascending limb of the loop of Henle (loop diuretic therapy) [3].
  • Starting from a model body weight for the rat of 200 g and considering the percentage of thin segments in the tissue of the renal pyramid, a loop of Henle with a length of 8.1 mm for the thin part and a length of 2.4 mm for the ascending thick limb was calculated for the model nephron from the lengths of the loops of the three types of nephrons [4].
  • Most patients with Bartter syndrome have defects in transporters in the thick ascending limb of the loop of Henle, such as the Na-K-2Cl cotransporter, NKCC2, or the ATP-sensitive potassium channel, ROMK [5].

High impact information on Loop of Henle

  • The distal tubule reabsorbs approximately 10% of the filtered Mg(2+), but this is 70-80% of that delivered from the loop of Henle [6].
  • Because the terminal nephron segments, including the DCT and collecting tubule, reabsorb only a small portion of the filtered Mg (approximately 5%), the loop of Henle plays a major role in the determination of Mg reabsorption, and it is in this segment that the major regulatory factors act to maintain Mg balance [7].
  • In accordance with the phenotype, BSND is expressed in the thin limb and the thick ascending limb of the loop of Henle in the kidney and in the dark cells of the inner ear [8].
  • The medullary portion of the thick ascending limb of the loop of Henle (mTALH) has one of the highest concentrations of (Na+ + K+)ATPase found in mammalian tissues, reflecting the importance of this nephron segment in the regulation of extracellular fluid volume, as active sodium transport is driven by (Na+ + K+)ATPase [9].
  • In the medullary segment of the thick ascending limb of the loop of Henle (mTALH), arachidonic acid (AA) is metabolized by a cytochrome P450-dependent monooxygenase to products that affect ion transport [10].

Chemical compound and disease context of Loop of Henle


Biological context of Loop of Henle

  • Effect of cytochrome P450 arachidonate metabolites on ion transport in rabbit kidney loop of Henle [10].
  • Tubular-fluid reabsorption by specialized cells of the nephron at the junction of the ascending limb of the loop of Henle and the distal convoluted tubule, termed the macula densa, releases compounds causing vasoconstriction of the adjacent afferent arteriole [12].
  • Moreover, site-specific delivery of HO-1 to renal structures in spontaneously hypertensive rats (SHR), specifically to the medullary thick ascending limb of the loop of Henle (mTALH), has been shown to normalize blood pressure and provide protection to the mTAL against oxidative injury [13].
  • In his hypothesis of the evolution of renal functions Homer Smith proposed that the formation of glomerular nephron and body armor had been adequate for the appearance of primitive vertebrates in fresh water and that the adaptation of homoiotherms to terrestrial life was accompanied by the appearance of the loop of Henle [14].
  • The present results indicate that tubular secretion of piretanide is important for the diuretic response and that piretanide inhibits the fluid absorption in the loop of Henle and the tubuloglomerular feedback control which would otherwise blunt the diuretic response with a reduction in glomerular filtration rate [15].

Anatomical context of Loop of Henle


Associations of Loop of Henle with chemical compounds

  • Agents acting in the loop of Henle that increase chloride excretion relative to sodium tend to cause greater calcium excretion [21].
  • Bicarbonate reabsorption that was insensitive to acetazolamide occurred in the superficial and deep loop of Henle and between the distal tubule and base collecting duct [22].
  • Similarly, the concentration gradient favoring transfer of NH3 between loop of Henle and CD was reduced in SAD [23].
  • The enzyme is present in most tissues and its possible physiological role is to produce an electrically neutral, non-diffusible osmolyte in cells exposed to hypertonicity, as typified by the renal medullary cells of the loop of Henlé. The enzyme has a low affinity for glucose, and under normal conditions it processes little substrate [24].
  • Recent studies have demonstrated that in vivo administration of 1-deamino-8-D-arginine-vasopressin, an analog of arginine-8-vasopressin, induces homologous desensitization to vasopressin in the thick ascending limb of the loop of Henle [25].

Gene context of Loop of Henle

  • We found that Hes5 is specifically expressed in the anlage of the loop of Henle, suggesting that it might be involved in the determination of its cell identity [26].
  • We conclude that Slc26a7 is expressed in the proximal tubule and thick ascending limb of the loop of Henle, and it may therefore contribute to anion transport in these nephron segments [27].
  • Dentin matrix protein-1 (DMP1) and MMP-9 were coexpressed throughout the nephron, including both parietal cells of Bowman's capsule and the thin limb of the loop of Henle [28].
  • The significance of mixed tumour cell expression of antigens specific for the proximal tubule (CD10, DPP4 and aminopeptidase N) and of Tamm Horsfall protein, normally expressed on the thick ascending limb of loop of Henle and distal tubule, is discussed [29].
  • COX-2 expression was also found in the cortical thick ascending limb of the loop of Henle (medullary rays and macula densa) in 50 of 53 cases [30].

Analytical, diagnostic and therapeutic context of Loop of Henle

  • The proximal tubular stop-flow pressure (PSF) was measured to estimate changes in PGC obtained after activation of the TGF system by varying the loop of Henle perfusion rate with artificial ultrafiltrate including vehicle, NOS inhibition or L-arginine [31].
  • NHE3 appears not to significantly contribute to fluid or Na(+) reabsorption in the loop of Henle (including the S3 segment of proximal tubule) or macula densa control of nephron filtration [32].
  • Western blot analysis exhibited relatively higher levels of HO-1 in isolated proximal tubules and relatively higher HO-2 levels in the thick ascending limbs of the loop of Henle and preglomerular arterioles [33].
  • Therefore, synthesis of Tamm-Horsfall protein (THP), a glycoprotein exclusively produced in the thick ascending limb of the loop of Henle, was measured by ELISA in the urine of seven infant HPS patients (aged 3 to 8 years) [34].
  • Indinavir crystallization around the loop of Henle: experimental evidence [35].


  1. Aquaretic agents: a new potential treatment of dilutional hyponatremia in cirrhosis. Ginès, P., Jiménez, W. J. Hepatol. (1996) [Pubmed]
  2. A study of the renal handling of water in lipoid nephrosis. Gur, A., Adefuin, P.Y., Siegel, N.J., Hayslett, J.P. Pediatr. Res. (1976) [Pubmed]
  3. Thiamin status, diuretic medications, and the management of congestive heart failure. Brady, J.A., Rock, C.L., Horneffer, M.R. Journal of the American Dietetic Association. (1995) [Pubmed]
  4. A geometric model of the rat kidney. Kainer, R. Anat. Embryol. (1975) [Pubmed]
  5. Concomitant occurrence of Gitelman and Bartter syndromes in the same family? Turman, M.A. Pediatr. Nephrol. (1998) [Pubmed]
  6. Magnesium transport in the renal distal convoluted tubule. Dai, L.J., Ritchie, G., Kerstan, D., Kang, H.S., Cole, D.E., Quamme, G.A. Physiol. Rev. (2001) [Pubmed]
  7. Renal magnesium handling and its hormonal control. de Rouffignac, C., Quamme, G. Physiol. Rev. (1994) [Pubmed]
  8. Mutation of BSND causes Bartter syndrome with sensorineural deafness and kidney failure. Birkenhäger, R., Otto, E., Schürmann, M.J., Vollmer, M., Ruf, E.M., Maier-Lutz, I., Beekmann, F., Fekete, A., Omran, H., Feldmann, D., Milford, D.V., Jeck, N., Konrad, M., Landau, D., Knoers, N.V., Antignac, C., Sudbrak, R., Kispert, A., Hildebrandt, F. Nat. Genet. (2001) [Pubmed]
  9. Renal cytochrome P450-related arachidonate metabolite inhibits (Na+ + K+)ATPase. Schwartzman, M., Ferreri, N.R., Carroll, M.A., Songu-Mize, E., McGiff, J.C. Nature (1985) [Pubmed]
  10. Effect of cytochrome P450 arachidonate metabolites on ion transport in rabbit kidney loop of Henle. Escalante, B., Erlij, D., Falck, J.R., McGiff, J.C. Science (1991) [Pubmed]
  11. The effects of respiratory alkalosis and acidosis on net bicarbonate flux along the rat loop of Henle in vivo. Unwin, R., Stidwell, R., Taylor, S., Capasso, G. Am. J. Physiol. (1997) [Pubmed]
  12. Nitric oxide synthase in macula densa regulates glomerular capillary pressure. Wilcox, C.S., Welch, W.J., Murad, F., Gross, S.S., Taylor, G., Levi, R., Schmidt, H.H. Proc. Natl. Acad. Sci. U.S.A. (1992) [Pubmed]
  13. Heme oxygenase and the cardiovascular-renal system. Abraham, N.G., Kappas, A. Free Radic. Biol. Med. (2005) [Pubmed]
  14. Evolutionary aspects of renal function. Natochin, Y.V. Kidney Int. (1996) [Pubmed]
  15. Renal tubular secretion of piretanide and its effects on electrolyte reabsorption and tubuloglomerular feedback mechanism. Odlind, B., Beermann, B., Selén, G., Persson, A.E. J. Pharmacol. Exp. Ther. (1983) [Pubmed]
  16. Expression of the human neuropeptide tyrosine Y1 receptor. Wharton, J., Gordon, L., Byrne, J., Herzog, H., Selbie, L.A., Moore, K., Sullivan, M.H., Elder, M.G., Moscoso, G., Taylor, K.M. Proc. Natl. Acad. Sci. U.S.A. (1993) [Pubmed]
  17. [3H]bumetanide binding to membranes isolated from dog kidney outer medulla. Relationship to the Na,K,Cl co-transport system. Forbush, B., Palfrey, H.C. J. Biol. Chem. (1983) [Pubmed]
  18. Calbindin-D9k and parvalbumin are exclusively located along basolateral membranes in rat distal nephron. Bindels, R.J., Timmermans, J.A., Hartog, A., Coers, W., van Os, C.H. J. Am. Soc. Nephrol. (1991) [Pubmed]
  19. Contribution of Na+-H+ exchange to sodium reabsorption in the loop of henle: a microperfusion study in rats. Shirley, D.G., Walter, S.J., Unwin, R.J., Giebisch, G. J. Physiol. (Lond.) (1998) [Pubmed]
  20. Expression of osteopontin, a urinary inhibitor of stone mineral crystal growth, in rat kidney. Kleinman, J.G., Beshensky, A., Worcester, E.M., Brown, D. Kidney Int. (1995) [Pubmed]
  21. Renal calcium metabolism and diuretics. Stier, C.T., Itskovitz, H.D. Annu. Rev. Pharmacol. Toxicol. (1986) [Pubmed]
  22. Effect of carbonic anhydrase inhibition on superficial and deep nephron bicarbonate reabsorption in the rat. DuBose, T.D., Lucci, M.S. J. Clin. Invest. (1983) [Pubmed]
  23. Effect of selective aldosterone deficiency on acidification in nephron segments of the rat inner medulla. DuBose, T.D., Caflisch, C.R. J. Clin. Invest. (1988) [Pubmed]
  24. Aldose reductase inhibitors and their potential for the treatment of diabetic complications. Tomlinson, D.R., Stevens, E.J., Diemel, L.T. Trends Pharmacol. Sci. (1994) [Pubmed]
  25. In vitro desensitization of isolated nephron segments to vasopressin. Dublineau, I., Pradelles, P., de Rouffignac, C., Elalouf, J.M. Proc. Natl. Acad. Sci. U.S.A. (1990) [Pubmed]
  26. Segmental expression of Notch and Hairy genes in nephrogenesis. Chen, L., Al-Awqati, Q. Am. J. Physiol. Renal Physiol. (2005) [Pubmed]
  27. Immunolocalization of anion transporter Slc26a7 in mouse kidney. Dudas, P.L., Mentone, S., Greineder, C.F., Biemesderfer, D., Aronson, P.S. Am. J. Physiol. Renal Physiol. (2006) [Pubmed]
  28. Renal expression of SIBLING proteins and their partner matrix metalloproteinases (MMPs). Ogbureke, K.U., Fisher, L.W. Kidney Int. (2005) [Pubmed]
  29. Tamm Horsfall protein expression by a small renal cell carcinoma presenting with metastases. Gaulier, A., Lucas, G., Ronco, P. Histopathology (1990) [Pubmed]
  30. Immunohistochemical expression of cyclooxygenase-2 in normal kidneys. Adegboyega, P.A., Ololade, O. Appl. Immunohistochem. Mol. Morphol. (2004) [Pubmed]
  31. Macula densa derived nitric oxide in regulation of glomerular capillary pressure. Thorup, C., Erik, A., Persson, G. Kidney Int. (1996) [Pubmed]
  32. Role of Na(+)/H(+) exchanger NHE3 in nephron function: micropuncture studies with S3226, an inhibitor of NHE3. Vallon, V., Schwark, J.R., Richter, K., Hropot, M. Am. J. Physiol. Renal Physiol. (2000) [Pubmed]
  33. Heme oxygenase isoform-specific expression and distribution in the rat kidney. da Silva, J.L., Zand, B.A., Yang, L.M., Sabaawy, H.E., Lianos, E., Abraham, N.G. Kidney Int. (2001) [Pubmed]
  34. Marked reduction of Tamm-Horsfall protein synthesis in hyperprostaglandin E-syndrome. Schröter, J., Timmermans, G., Seyberth, H.W., Greven, J., Bachmann, S. Kidney Int. (1993) [Pubmed]
  35. Indinavir crystallization around the loop of Henle: experimental evidence. Dieleman, J.P., Salahuddin, S., Hsu, Y.S., Burger, D.M., Gyssens, I.C., Sturkenboom, M.C., Stricker, B.H., Kok, D.J. J. Acquir. Immune Defic. Syndr. (2001) [Pubmed]
WikiGenes - Universities