Tubular epithelial cells

Endothelial NO Synthase (eNOS) expression is relatively specific for endothelial cells. However, the isozyme has also been detected in certain neurons of the brain, in syncytiotrophoblasts of human placenta and in LLC-PKi kidney tubular epithelial cells. 

F (shrunken glomerular tufts necrosis of tubular epithelial cells)... 

Ueda, N. and Shah, S.V. (1992). Endonuclease-induced DNA damage and cell death in oxidant injury to renal tubular epithelial cells. J. Clin. Invest. 90, 2593-2597. 

Renal Effects. The characteristics of early or acute lead-induced nephropathy in humans include nuclear inclusion bodies, mitochondrial changes, and cytomegaly of the proximal tubular epithelial cells dysfunction of the proximal tubules (Fanconi s syndrome) manifested as aminoaciduria, glucosuria, and phosphaturia with hypophosphatemia and increased sodium and decreased uric acid excretion. These effects appear to be reversible. Characteristics of chronic lead nephropathy include progressive interstitial fibrosis, dilation of tubules and atrophy or hyperplasia of the tubular epithelial cells, and few or no nuclear inclusion bodies, reduction in glomerular filtration rate, and azotemia. These effects are irreversible. The acute form is reported in lead-intoxicated children, whose primary exposure is via the oral route, and sometimes in lead workers. The chronic form is reported mainly in lead workers, whose primary exposure is via inhalation. Animal studies provide evidence of nephropathy similar to that which occurs in humans, particularly the acute form (see Section 2.2.3.2). 

Active reabsorption occurs when the movement of a given substance across the luminal surface or the basolateral surface of the tubular epithelial cell requires energy. Substances that are actively reabsorbed from the tubule include glucose amino acids and Na+, POy3, and Ca++ ions. Three generalizations can be made regarding the tubular reabsorption of sodium, chloride, and water ... 

Reabsorption of Na+ ions is an active process 80% of the total energy expended by the kidneys is used for sodium transport out of the tubular epithelial cell. 

Sodium reabsorption. Sodium is reabsorbed by different mechanisms as the filtrate progresses through the tubule. Sodium ions leave the filtrate and enter the tubular epithelial cell by way of the following processes (see Figure 19.4) ... 

More simply, in the early regions of the tubule (proximal tubule and Loop of Henle), Na+ ions leave the lumen and enter the tubular epithelial cells by way of passive facilitated transport mechanisms. The diffusion of Na+ ions is coupled with organic molecules or with other ions that electrically balance the flux of these positively charged ions. In the latter regions of the tubule (distal tubule and collecting duct), Na+ ions diffuse into the epithelial cells through Na+ channels. 

Formation of Na+ channels in the luminal membrane of the tubular epithelial cells (facilitates passive diffusion of Na+ ions into the cell)... 

Formation of Na+, K+-ATPase carrier molecules in the basolateral membrane of the tubular epithelial cells (promotes extrusion of Na+ ions from the cells and their movement into plasma by way of peritubular capillaries enhances the concentration gradient for passive diffusion through Na+ channels in the luminal membrane)... 

Most of the CP ions diffuse between the tubular epithelial cells. 

Water reabsorption. Water is reabsorbed passively by way of osmosis from many regions of the tubule. As with sodium and chloride, 65% of the filtered water is reabsorbed from the proximal tubule. An additional 15% of the filtered water is reabsorbed from the descending limb of the Loop of Henle. This reabsorption occurs regardless of the water content of the body. The water enters the tubular epithelial cells through water channels, also referred to as aquaporins. These channels are always open in the early regions of the tubule. 

Because the transport of sodium is an active process, it is used to accumulate NaCl in the interstitial fluid of the medulla. In fact, this activity is involved in the initial establishment of the vertical osmotic gradient. Furthermore, sodium is actively transported out of the tubular epithelial cells up its concentration gradient until the filtrate is 200 mOsm/1 less concentrated than the surrounding interstitial fluid. This difference between the filtrate and the interstitial fluid is referred to as the horizontal osmotic gradient. Because the filtrate at the end of the Loop of Henle has an osmolarity of 100 mOsm/1, the kidneys have the ability to produce urine that is significantly more dilute than the plasma. 

Carbonic anhydrase inhibitors such as acetazolamide act in the proximal tubule. These drugs prevent the formation of H+ ions, which are transported out of the tubular epithelial cell in exchange for Na+ ions. These agents have limited clinical usefulness because they result in development of metabolic acidosis. 

Potassium ion secretion. Potassium ions are secreted in the distal tubule and the collecting duct. These ions diffuse down their concentration gradient from the peritubular capillaries into the interstitial fluid. They are then actively transported up their concentration gradient into the tubular epithelial cells by way of the Na+, K+ pump in the basolateral membrane. Finally, potassium ions exit the epithelial cells by passive diffusion through K+ channels in the luminal membrane and enter tubular fluid to be excreted in the urine. 

Colon adenocarcinoma epithelial cell line Rat renal proximal tubular epithelial cell line Tetrahydrofuranyl Valacyclovir hydrolase... 

Tubular epithelial cell damage Acute tubular necrosis Pentamidine... 

Acute-, intermediate-, and chronic-duration oral exposures of male rats to doses of 10 mg/kg/day or greater were associated with renal tubular nephropathy (Gorzinski et al. 1985 NTP 1977, 1989 Weeks et al. 1979). Affected animals displayed tubular necrosis, hyaline droplets in tubular epithelial cells, regenerative tubular epithelium, interstitial nephritis, and fibrosis. The severity of the renal lesions varied with the dose and the duration of exposure. 

After peroral intake of nickel sulphate in mice, kidney damage appeared at the corticomedullary junction [296]. There was loss of renal tubular epithelial cells and protein loss, giving numerous hyaline casts in the renal tubules and collecting ducts, especially prominent in the renal papillae. 

Eurell TE, Eurell JC, Schaeffer DJ, et al Lysosomal changes in renal proximal tubular epithelial cells of male Sprague Dawley rats following decalin exposure. Toxicol Pathol 18 637-642, 1990... 

Exposure to tetralin-saturated vapor for 8 hours was lethal to rats. Nephrotoxicity, evidenced as increased cytoplasmic hyalin droplets in proximal convoluted tubular epithelial cells, occurred in male but not female rats exposed intragastrically for 2 weeks." ... 

This chapter is divided into three sections. The first section covers renal tubule transport mechanisms. The nephron is divided structurally and functionally into several segments (Figure 15-1, Table 15-1). Many diuretics exert their effects on specific membrane transport proteins in renal tubular epithelial cells. Other diuretics exert osmotic effects that prevent water reabsorption (mannitol), inhibit enzymes (acetazolamide), or interfere with hormone receptors in renal epithelial cells (aldosterone receptor blockers). The physiology of each segment is closely linked to the basic pharmacology of the drugs acting there, which is discussed in the second section. Finally, the clinical applications of diuretics are discussed in the third section. 

Mineralocorticoids are believed to increase sodium reabsorption by affecting sodium channels and sodium pumps on the epithelial cells lining the renal tubules.18,58 Mineralocorticoids ability to increase the expression of sodium channels is illustrated in Figure 29-5. These hormones enter the tubular epithelial cell, bind to receptors in the cell, and create an activated hormone-receptor complex.18 This complex then travels to the nucleus to initiate transcription of messenger RNA units, which are translated into specific membrane-related proteins.27,58 These proteins in some way either create or help open sodium pores on the cell membrane, thus allowing sodium to leave the tubule and enter the epithelial cell by passive diffusion.27,83 Sodium is then actively transported out of the cell and reabsorbed into the bloodstream. Water reabsorption is increased as water follows the sodium movement back into the bloodstream. As sodium is reabsorbed, potassium is secreted by a sodium-potassium exchange, thus increasing potassium excretion (see Fig. 29-5). 

Hughes, D. (1990) Immunocytochemistry—selecting a procedure for the identification of vascular endothelial and tubular epithelial cells aspirated from human renal allografts. Trans. R. M. S. 1, 701-706. 

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