scholarly journals Role of 20-HETE in Elevating Chloride Transport in the Thick Ascending Limb of Dahl SS/Jr Rats

Hypertension ◽  
1999 ◽  
Vol 33 (1) ◽  
pp. 419-423 ◽  
Author(s):  
Osamu Ito ◽  
Richard J. Roman
Keyword(s):  
Chloride Transport ◽  
Thick Ascending Limb

The role of chloride transport in postsynaptic inhibition of hippocampal neurons

Science ◽  
1986 ◽  
Vol 232 (4756) ◽  
pp. 1413-1415 ◽  
Author(s):  
U Misgeld ◽  
R. Deisz ◽  
H. Dodt ◽  
H. Lux
Keyword(s):  
Hippocampal Neurons ◽  
Chloride Transport ◽  
Postsynaptic Inhibition

MO092THE ROLE OF CALCIUM IN UROMODULIN EXPRESSION AND SECRETION FROM RENAL MEDULLARY EPITHELIAL CELLS OF HYPERTENSIVE AND NORMOTENSIVE RATS

2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
Philipp Boder ◽  
Sheon Mary ◽  
Lesley Graham ◽  
Christian Delles
Keyword(s):  
Blood Pressure ◽  
Epithelial Cells ◽  
Mrna Level ◽  
Extracellular Calcium ◽  
Female Rats ◽  
Thick Ascending Limb ◽  
Molecular Signaling ◽  
Extracellular Secretion ◽  
Wistar Kyoto

Abstract Background and Aims Uromodulin (UMOD) is the most abundantly secreted protein found within the urine, primarily produced by medullary thick ascending limb (mTAL) epithelial cells of the kidneys. There is accruing genetic evidence implicating UMOD in blood pressure regulation and consequently hypertension. The molecular signaling induced by calcium in the kidney and its influence on blood pressure are not well understood. The aim of this study was to investigate the potential role of extracellular calcium and the calcium-sensing receptor (CaSR) in mTAL on UMOD production and secretion in TAL cells with the hope of defining novel clinical targets for the treatment of hypertension. Method Kidneys were harvested from normotensive Wistar-Kyoto (WKY) and stroke-prone spontaneously hypertensive (SHRSP) female rats. To determine the effect of extracellular calcium on UMOD secretion, mTAL tubules were incubated in media with and without 1mM calcium, nifedipine (10µM), NPS2143 (1 or 5 µM) and spermine (2mM). Extracellular and intracellular UMOD protein levels were detected by Western blot. Gene expression of Umod was determined by qRT-PCR. Results Calcium increased mTAL tubule UMOD secretion in WKY and SHRSP. Nifedipine slightly decreased UMOD secretion in WKY without calcium. In both strains, NPS2143 increased calcium-induced UMOD secretion, with an enhanced effect in SHRSP. Stimulation of CaSR with spermine decreased UMOD secretion in WKY. Analysis of intracellular UMOD levels in these conditions demonstrated increased accumulation when extracellular secretion was low, and vice versa. Incubation of primary mTAL cells with calcium confirmed increased localisation of UMOD at the membrane compared to the cytosol, without any major differences in cell morphology. The Umod mRNA level changes were not statistically significant among conditions. Conclusion Trafficking of UMOD in the mTAL is influenced by the type of CaSR ligand and the biased nature of G-protein coupled CaSR signalling. Unravelling the signalling events post-calcium will be necessary for identification of key regulators of UMOD secretion and provide new sites for therapeutic intervention in hypertension.

scholarly journals Expression and role of serum and glucocorticoid-regulated kinase 2 in the regulation of Na+/H+ exchanger 3 in the mammalian kidney

2010 ◽  
Vol 299 (6) ◽  
pp. F1496-F1506 ◽  
Author(s):  
Alan C. Pao ◽  
Aditi Bhargava ◽  
Francesca Di Sole ◽  
Raymond Quigley ◽  
Xinli Shao ◽  
...  
Keyword(s):  
In Situ Hybridization ◽  
Proximal Tubule ◽  
Cell Surface Expression ◽  
Thick Ascending Limb ◽  
Proximal Tubule Cells ◽  
Mammalian Kidney ◽  
Tubule Cells ◽  
Exchange Activity

Serum and glucocorticoid-regulated kinase 2 (sgk2) is 80% identical to the kinase domain of sgk1, an important mediator of mineralocorticoid-regulated sodium (Na+) transport in the distal nephron of the kidney. The expression pattern and role in renal function of sgk2 are virtually uncharacterized. In situ hybridization and immunohistochemistry of rodent kidney coupled with real-time RT-PCR of microdissected rat kidney tubules showed robust sgk2 expression in the proximal straight tubule and thick ascending limb of the loop of Henle. Sgk2 expression was minimal in distal tubule cells with aquaporin-2 immunostaining but significant in proximal tubule cells with Na+/H+ exchanger 3 (NHE3) immunostaining. To ascertain whether mineralocorticoids regulate expression of sgk2 in a manner similar to sgk1, we examined sgk2 mRNA expression in the kidneys of adrenalectomized rats treated with physiological doses of aldosterone together with the glucocorticoid receptor antagonist RU486. Northern blot analysis and in situ hybridization showed that, unlike sgk1, sgk2 expression in the kidney was not altered by aldosterone treatment. Based on the observation that sgk2 is expressed in proximal tubule cells that also express NHE3, we asked whether sgk2 regulates NHE3 activity. We heterologously expressed sgk2 in opossum kidney (OKP) cells and measured Na+/H+ exchange activity by Na+-dependent cell pH recovery. Constitutively active sgk2, but not sgk1, stimulated Na+/H+ exchange activity by >30%. Moreover, the sgk2-mediated increase in Na+/H+ exchange activity correlated with an increase in cell surface expression of NHE3. Together, these results suggest that the pattern of expression, regulation, and role of sgk2 within the mammalian kidney are distinct from sgk1 and that sgk2 may play a previously unrecognized role in the control of transtubular Na+ transport through NHE3 in the proximal tubule.

scholarly journals Potential role of luminal potassium in tubuloglomerular feedback.

1997 ◽  
Vol 8 (12) ◽  
pp. 1831-1837 ◽  
Author(s):  
V Vallon ◽  
H Osswald ◽  
R C Blantz ◽  
S Thomson
Keyword(s):  
Potential Role ◽  
Macula Densa ◽  
Tubuloglomerular Feedback ◽  
K Channel ◽  
Thick Ascending Limb ◽  
Retrograde Perfusion ◽  
Luminal Membrane ◽  
K Concentration ◽  
Tubular Flow

Transport through the Na+-2Cl(-)-K+ cotransporter in the luminal membrane of macula densa cells is considered critical for tubuloglomerular feedback (TGF). Although various studies could support the importance of luminal Na+ and Cl-, the role of luminal K+ in TGF has not been thoroughly addressed. The study presented here examines this issue in nephrons with superficial glomeruli of anesthetized male Munich-Wistar-Frömter rats. Ambient Na+ concentration in early distal tubular fluid was approximately 22 mM, suggesting collection sites relatively close to the macula densa segment. First, it was found that ambient early distal tubular K+ concentration is approximately 1.3 mM, i.e., close to the K+ affinity of the Na+-2Cl(-)-K+ cotransporter in the thick ascending limb. Second, it was observed that a change in late proximal tubular flow rate, i.e., a maneuver that is known to induce a TGF response, significantly alters early distal tubular K+ concentration. Third, previous experiments failed to show an inhibition in TGF response during retrograde perfusion of the macula densa with K+-free solutions. Because of a potential K+ influx into the lumen between the perfusion site and the macula densa, however, the K+ channel blocker U37883A was added to the K+-free perfusate. TGF response was assessed as the fall in nephron filtration rate in response to retrograde perfusion of the macula densa segment from early distal tubular site. It was observed that luminal U37883A (100 microM) significantly attenuated TGF. Because adding 5 mM KCl to the perfusate restored TGF in the presence of U37883A and because the inhibitory action of U37883A on tubular K+ secretion was confirmed, the effect of U37883A on TGF was most likely caused by inhibition of K+ influx into the perfused segment, which decreased luminal K+ concentration at the macula densa. The present findings support a potential role for luminal K+ in TGF, which is in accordance with a transmission of the TGF signal across the macula densa via Na+-2Cl(-)-K+ cotransporter.

scholarly journals 3P-209 Role of Asp252 in chloride transport by pharaonis halorhodopsin(Photobiology:Vision & Photoreception,The 47th Annual Meeting of the Biophysical Society of Japan)

2009 ◽  
Vol 49 (supplement) ◽  
pp. S186
Author(s):  
Takashi Kikukawa ◽  
Seiji Miyauchi ◽  
Hiroaki Ichio ◽  
Taku Kitagawa ◽  
Makoto Demura ◽  
...  
Keyword(s):  
Annual Meeting ◽  
Chloride Transport ◽  
Biophysical Society

Neo-Mull-Soy Metabolic Alkalosis: A Model of Bartter's Syndrome?

PEDIATRICS ◽  
1980 ◽  
Vol 66 (5) ◽  
pp. 784-786
Author(s):  
Vivian M. Reznik ◽  
William R. Griswold ◽  
Stanley A. Mendoza ◽  
Richard M. McNeal
Keyword(s):  
Metabolic Alkalosis ◽  
Chloride Transport ◽  
Chloride Concentration ◽  
Thick Ascending Limb ◽  
Loop Of Henle ◽  
Bartter’S Syndrome ◽  
Bartter's Syndrome ◽  
Hypokalemic Alkalosis

A case of Neo-Mull-Soy-induced metabolic alkalosis occurred in an 8-month-old child. This child had hypochloremic hypokalemic alkalosis as well as hyperreninemia. Initially, a diagnosis of Bartter's syndrome was made and treatment consisted of KCl replacement, indomethacin, and aspirin. In retrospect, the diagnosis of Neo-Mull-Soy induced metabolic alkalosis could have been suspected on the basis of the low chloride concentration in his urine. Proposed mechanisms for the etiology of Bartter's syndrome are reviewed. Neo-Mull-Soy induced metabolic alkalosis simulates Bartter's syndrome and supports the concept that the primary abnormality in Bartter's syndrome is chloride deficiency. The chloride deficiency in Bartter's syndrome results from a defect in active chloride transport in the thick ascending limb of the loop of Henle.

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