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

• We have studied the effects of acute respiratory alkalosis (ARALK, hyperventilation) and acidosis (ARA, 8% CO2), chronic respiratory acidosis (CRA; 10% CO2 for 7-10 days), and subsequent recovery from CRA breathing air on loop of Henle (LOH) net bicarbonate flux (JHCO3) by in vivo tubule microperfusion in anesthetized rats [11].

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

• Y1 receptor mRNA was detected in renal collecting ducts, loop of Henle, and juxtaglomerular apparatus and in the syncytiotrophoblast layer of placental villi [16].
• On sucrose gradient centrifugation, a peak of [3H]bumetanide binding activity (30 pmol/mg) is obtained at 37% (w/v) sucrose, distinct from the basolateral membranes in outer medulla and from brush borders in proximal tubule; our hypothesis is that this peak contains luminal membranes from the thick ascending limb of the loop of Henle [17].
• In rat kidney cortex, parvalbumin and calbindin-D9k colocalized in the thick ascending loop of Henle, the distal convoluted tubule, the connecting tubule, and the intercalated cells of the collecting duct [18].
• 1. The contribution of apical Na+-H+ exchange to sodium reabsorption in the thick ascending limb of the loop of Henle (TALH) in vivo was examined in anaesthetized rats by perfusing loops of Henle of superficial nephrons with solutions containing the Na+-H+ exchange inhibitor, ethyl isopropyl amiloride (EIPA) [19].
• Fluorescence, confocal and electron microscopy revealed osteopontin primarily in cells of the descending thin limb of the loop of Henle (DTL) and in papillary surface epithelium (PSE) in the area of the calyceal fornix [20].

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].

References