The Experts below are selected from a list of 234 Experts worldwide ranked by ideXlab platform
David H. Ellison - One of the best experts on this subject based on the ideXlab platform.
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Distal Convoluted Tubule sexual dimorphism revealed by advanced 3D imaging
American journal of physiology. Renal physiology, 2020Co-Authors: Ebrahim Tahaei, David H. Ellison, Richard Coleman, Turgay Saritas, Paul A. WellingAbstract:The thiazide-sensitive Na+-Cl− cotransporter (NCC) is more abundant in kidneys of female subjects than of male subjects. Because morphological remodeling of the distal Convoluted Tubule (DCT) is de...
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distal Convoluted Tubule cl concentration is modulated via k channels and transporters
American Journal of Physiology-renal Physiology, 2020Co-Authors: Nathan J Klett, Wen Hui Wang, Avika Sharma, Charles N Allen, Chao Ling Yang, David H. EllisonAbstract:Cl−-sensitive with-no-lysine kinase (WNK) plays a key role in regulating the thiazide-sensitive Na+-Cl− cotransporter (NCC) in the distal Convoluted Tubule (DCT). Cl− enters DCT cells through NCC a...
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Effect of Angiotensin II on ENaC in the Distal Convoluted Tubule and in the Cortical Collecting Duct of Mineralocorticoid Receptor Deficient Mice
Journal of the American Heart Association, 2020Co-Authors: Zhong Xiuzi Gao, David H. Ellison, Andrew S. Terker, Dan-dan Zhang, Xin Peng Duan, Dao Hong Lin, Wen Hui WangAbstract:Background Angiotensin II stimulates epithelial Na+ channel (ENaC) by aldosterone‐independent mechanism. We now test the effect of angiotensin II on ENaC in the distal Convoluted Tubule (DCT) and c...
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Distal Convoluted Tubule.
Comprehensive Physiology, 2014Co-Authors: James A. Mccormick, David H. EllisonAbstract:The distal Convoluted Tubule (DCT) is a short nephron segment, interposed between the macula densa and collecting duct. Even though it is short, it plays a key role in regulating extracellular fluid volume and electrolyte homeostasis. DCT cells are rich in mitochondria, and possess the highest density of Na+/K+-ATPase along the nephron, where it is expressed on the highly amplified basolateral membranes. DCT cells are largely water impermeable, and reabsorb sodium and chloride across the apical membrane via electroneurtral pathways. Prominent among this is the thiazide-sensitive sodium chloride cotransporter, target of widely used diuretic drugs. These cells also play a key role in magnesium reabsorption, which occurs predominantly, via a transient receptor potential channel (TRPM6). Human genetic diseases in which DCT function is perturbed have provided critical insights into the physiological role of the DCT, and how transport is regulated. These include Familial Hyperkalemic Hypertension, the salt-wasting diseases Gitelman syndrome and EAST syndrome, and hereditary hypomagnesemias. The DCT is also established as an important target for the hormones angiotensin II and aldosterone; it also appears to respond to sympathetic-nerve stimulation and changes in plasma potassium. Here, we discuss what is currently known about DCT physiology. Early studies that determined transport rates of ions by the DCT are described, as are the channels and transporters expressed along the DCT with the advent of molecular cloning. Regulation of expression and activity of these channels and transporters is also described; particular emphasis is placed on the contribution of genetic forms of DCT dysregulation to our understanding.
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distal Convoluted Tubule
Clinical Journal of The American Society of Nephrology, 2014Co-Authors: Arohan R Subramanya, David H. EllisonAbstract:The distal Convoluted Tubule is the nephron segment that lies immediately downstream of the macula densa. Although short in length, the distal Convoluted Tubule plays a critical role in sodium, potassium, and divalent cation homeostasis. Recent genetic and physiologic studies have greatly expanded our understanding of how the distal Convoluted Tubule regulates these processes at the molecular level. This article provides an update on the distal Convoluted Tubule, highlighting concepts and pathophysiology relevant to clinical practice.
Herve Favre - One of the best experts on this subject based on the ideXlab platform.
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modulation of na k atpase activity by a tyrosine phosphorylation process in rat proximal Convoluted Tubule
The Journal of Physiology, 1997Co-Authors: Eric Feraille, Maria Luisa Carranza, Martine Rousselot, Herve FavreAbstract:1. In the rat kidney proximal Convoluted Tubule, epidermal growth factor and insulin have been reported to stimulate Na+ reabsorption. Because most of the effects of these growth factors are mediated by a process of tyrosine phosphorylation and Na+,K(+)-ATPase drives Na+ reabsorption, the influence of tyrosine kinases and tyrosine phosphatases on Na+,K(+)-ATPase activity located in the proximal Convoluted Tubule was evaluated. 2. Activation of receptor tyrosine kinases by epidermal growth factor and insulin stimulated ouabain-sensitive 86Rb+ uptake. The effects of epidermal growth factor and insulin were prevented by genistein, a tyrosine kinase inhibitor, but were unaffected by GF109203X, a protein kinase C inhibitor. 3. Inhibition of tyrosine phosphatases by orthovanadate (10(-7) and 10(-6)M) mimicked the effects of activation of receptor tyrosine kinases: stimulation of the ouabain-sensitive 86Rb+ uptake and of the hydrolytic activity of Na+,K(+)-ATPase under rate-limiting Na+ concentration, and absence of modification of the maximal activity (Vmax) of the enzyme. The effects of orthovanadate and insulin on the ouabain-sensitive 86Rb+ uptake were not additive. 4. The present results show that both activation of receptor tyrosine kinases and inhibition of tyrosine phosphatases stimulate the Na+,K(+)-ATPase activity through a common mechanism. Thus, a tyrosine phosphorylation process directly controls the Na+,K(+)-ATPase activity and contributes to the physiological control of water and solute reabsorption in the proximal Convoluted Tubule.
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Modulation of Na+,K(+)-ATPase activity by a tyrosine phosphorylation process in rat proximal Convoluted Tubule.
The Journal of Physiology, 1997Co-Authors: Eric Feraille, Maria Luisa Carranza, Martine Rousselot, Herve FavreAbstract:1. In the rat kidney proximal Convoluted Tubule, epidermal growth factor and insulin have been reported to stimulate Na+ reabsorption. Because most of the effects of these growth factors are mediated by a process of tyrosine phosphorylation and Na+,K(+)-ATPase drives Na+ reabsorption, the influence of tyrosine kinases and tyrosine phosphatases on Na+,K(+)-ATPase activity located in the proximal Convoluted Tubule was evaluated. 2. Activation of receptor tyrosine kinases by epidermal growth factor and insulin stimulated ouabain-sensitive 86Rb+ uptake. The effects of epidermal growth factor and insulin were prevented by genistein, a tyrosine kinase inhibitor, but were unaffected by GF109203X, a protein kinase C inhibitor. 3. Inhibition of tyrosine phosphatases by orthovanadate (10(-7) and 10(-6)M) mimicked the effects of activation of receptor tyrosine kinases: stimulation of the ouabain-sensitive 86Rb+ uptake and of the hydrolytic activity of Na+,K(+)-ATPase under rate-limiting Na+ concentration, and absence of modification of the maximal activity (Vmax) of the enzyme. The effects of orthovanadate and insulin on the ouabain-sensitive 86Rb+ uptake were not additive. 4. The present results show that both activation of receptor tyrosine kinases and inhibition of tyrosine phosphatases stimulate the Na+,K(+)-ATPase activity through a common mechanism. Thus, a tyrosine phosphorylation process directly controls the Na+,K(+)-ATPase activity and contributes to the physiological control of water and solute reabsorption in the proximal Convoluted Tubule.
Rui-lan Gong - One of the best experts on this subject based on the ideXlab platform.
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PGF2α stimulates the 10-pS Cl− channel and thiazide-sensitive Na+-Cl− cotransporter in the distal Convoluted Tubule
American journal of physiology. Renal physiology, 2020Co-Authors: Lijun Wang, Yu Xiao, Jing Fang, Jun-lin Wang, Hao Zhang, Xin-xin Meng, Rui-lan GongAbstract:We used patch-clamp and Western blot analysis to test whether PGF2α stimulates the basolateral 10-pS Cl− channel and thiazide-sensitive Na+-Cl− cotransporter (NCC) in the distal Convoluted Tubule (...
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pgf2α stimulates the 10 ps cl channel and thiazide sensitive na cl cotransporter in the distal Convoluted Tubule
American Journal of Physiology-renal Physiology, 2020Co-Authors: Lijun Wang, Yu Xiao, Jing Fang, Jun-lin Wang, Hao Zhang, Xin-xin Meng, Rui-lan GongAbstract:We used patch-clamp and Western blot analysis to test whether PGF2α stimulates the basolateral 10-pS Cl− channel and thiazide-sensitive Na+-Cl− cotransporter (NCC) in the distal Convoluted Tubule (...
Richard P Lifton - One of the best experts on this subject based on the ideXlab platform.
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SeSAME/EAST syndrome--phenotypic variability and delayed activity of the distal Convoluted Tubule.
Pediatric Nephrology, 2012Co-Authors: Ute I Scholl, Haatal B. Dave, James A. Listman, Anita Farhi, Carol Nelson-williams, Ming Lu, Richard P LiftonAbstract:Background Mutations in the K+ channel KCNJ10 (Kir4.1) cause an autosomal recessive syndrome featuring seizures, sensorineural deafness, ataxia, mental retardation, and electrolyte imbalance (SeSAME). Kir4.1 localizes to the basolateral membrane of the renal distal Convoluted Tubule, and its loss of function mimics renal features of Gitelman syndrome, with hypokalemic alkalosis, hypomagnesemia, and hypocalciuria. Presentation early in life due to seizures provides an opportunity to investigate the development of the electrolyte defect with age.
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sesame east syndrome phenotypic variability and delayed activity of the distal Convoluted Tubule
Pediatric Nephrology, 2012Co-Authors: Ute I Scholl, Haatal B. Dave, James A. Listman, Anita Farhi, Carol Nelsonwilliams, Richard P LiftonAbstract:Background Mutations in the K+ channel KCNJ10 (Kir4.1) cause an autosomal recessive syndrome featuring seizures, sensorineural deafness, ataxia, mental retardation, and electrolyte imbalance (SeSAME). Kir4.1 localizes to the basolateral membrane of the renal distal Convoluted Tubule, and its loss of function mimics renal features of Gitelman syndrome, with hypokalemic alkalosis, hypomagnesemia, and hypocalciuria. Presentation early in life due to seizures provides an opportunity to investigate the development of the electrolyte defect with age.
Raymond Quigley - One of the best experts on this subject based on the ideXlab platform.
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inhibition of proximal Convoluted Tubule transport by dopamine
Kidney International, 1998Co-Authors: Michel Baum, Raymond QuigleyAbstract:Inhibition of proximal Convoluted Tubule transport by dopamine. Background Dopamine can produce a natriuresis and diuresis independent of changes in renal hemodynamics. However, previous studies have failed to demonstrate an inhibition of transport by dopamine in intact proximal Convoluted Tubules. Methods Rabbit proximal Convoluted Tubules were perfused in vitro with an ultrafiltrate-like solution and bathed in a serum-like albumin solution. Results In the present study, the addition of 10 -5 m dopamine to the lumen or bath of proximal Convoluted Tubules perfused in vitro had no effect on transport. In proximal Convoluted Tubules, addition of 10 -6 m bath norepinephrine increased the rate of volume absorption from 0.65 ± 0.08 to 0.93 ± 0.08nl/mm · min ( P -5 m luminal dopamine in the presence of bath norepinephrine inhibited the rate of volume absorption to 0.72 ± 0.10nl/mm · min ( P = 0.01). The inhibition in the rate of volume absorption by luminal dopamine in the presence of bath norepinephrine was completely blocked by the DA 1 antagonist, SCH 23390. The DA 1 agonist luminal 10 -5 m fenoldopam also inhibited volume absorption in the presence of bath norepinephrine, but the DA 2 agonist luminal 10 -5 m quinpirole was without effect. Bath 10 -5 m dopamine had no effect on volume absorption in the presence of bath norepinephrine. Conclusion Dopamine has no direct epithelial action on the proximal Convoluted Tubule. However, luminal dopamine antagonizes the stimulation in transport produced by norepinephrine. These studies suggest that luminal dopamine may play a role to modulate sodium transport in the presence of renal nerve activity.
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effect of luminal angiotensin ii on rabbit proximal Convoluted Tubule bicarbonate absorption
American Journal of Physiology-renal Physiology, 1997Co-Authors: Michel Baum, Raymond Quigley, Albert QuanAbstract:The present in vitro microperfusion study examined the effect of luminal angiotensin II on proximal Convoluted Tubule (PCT) volume absorption and bicarbonate transport. Neither 10−11 M, 10−10 M, no...
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Stimulation of proximal Convoluted Tubule phosphate transport by epidermal growth factor: signal transduction
American Journal of Physiology-Renal Physiology, 1995Co-Authors: Raymond Quigley, Donald A. Kennerly, Ji Nan Sheu, Michel BaumAbstract:The present study investigated the signal-transduction pathway responsible for the epidermal growth factor (EGF) stimulation of phosphate transport (JPhos) in the rabbit proximal Convoluted Tubule ...
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glucocorticoids stimulate rabbit proximal Convoluted Tubule acidification
Journal of Clinical Investigation, 1993Co-Authors: Michel Baum, Raymond QuigleyAbstract:Abstract Glucocorticoids have an important role in renal acidification; however, a direct effect of glucocorticoids on proximal Convoluted Tubule (PCT) acidification has not been directly demonstrated. In the present in vitro microperfusion study PCT from animals receiving dexamethasone (600 micrograms/kg twice daily for 2 d and 2 h before killing) had a significantly higher rate of bicarbonate absorption than did controls (92.0 +/- 13.3 vs 59.9 +/- 3.2 pmol/mm.min, P < 0.01). To examine if glucocorticoids had a direct epithelial action, dexamethasone was added to the bath of PCT perfused in vitro. After 3 h of incubation in paired experiments 10(-6) M and 10(-5) M dexamethasone resulted in an approximately 30% stimulation in the rate of bicarbonate absorption. 10(-7) M dexamethasone and 10(-6) M aldosterone had no effect on bicarbonate absorption. The stimulation of acidification by 10(-5) M dexamethasone was blocked by actinomycin D and cycloheximide. These data are consistent with a direct effect of glucocorticoids on PCT acidification, and this effect is dependent upon protein synthesis.
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prenatal glucocorticoids stimulate neonatal juxtamedullary proximal Convoluted Tubule acidification
American Journal of Physiology-renal Physiology, 1991Co-Authors: Michel Baum, Raymond QuigleyAbstract:The rate of neonatal proximal Convoluted Tubule (PCT) HCO3 absorption is lower than that of adult animals. The present in vitro microperfusion study examined whether prenatal dexamethasone (60 micr...