scholarly journals Pressure Control of Sodium Reabsorption and Intercellular Backflux across Proximal Kidney Tubule

1974 ◽  
Vol 54 (1) ◽  
pp. 69-82 ◽  
Author(s):  
Alain Grandchamp ◽  
Emile L. Boulpaep
Keyword(s):  
Pressure Control ◽  
Sodium Reabsorption ◽  
Kidney Tubule ◽  
Proximal Kidney Tubule

scholarly journals Interaction between Epithelial Sodium Channel γ-Subunit and Claudin-8 Modulates Paracellular Sodium Permeability in Renal Collecting Duct

2020 ◽  
Vol 31 (5) ◽  
pp. 1009-1023 ◽  
Author(s):  
Ali Sassi ◽  
Yubao Wang ◽  
Alexandra Chassot ◽  
Olga Komarynets ◽  
Isabelle Roth ◽  
...  
Keyword(s):  
Sodium Channel ◽  
Knockout Mice ◽  
Collecting Duct ◽  
Epithelial Sodium Channel ◽  
Paracellular Permeability ◽  
Sodium Reabsorption ◽  
Kidney Tubule ◽  
Sodium Permeability ◽  
Tubular Lumen ◽  
Renal Collecting Duct

BackgroundWater and solute transport across epithelia can occur via the transcellular or paracellular pathways. Tight junctions play a key role in mediating paracellular ion reabsorption in the kidney. In the renal collecting duct, which is a typical absorptive tight epithelium, coordination between transcellular sodium reabsorption and paracellular permeability may prevent the backflow of reabsorbed sodium to the tubular lumen along a steep electrochemical gradient.MethodsTo investigate whether transcellular sodium transport controls tight-junction composition and paracellular permeability via modulating expression of the transmembrane protein claudin-8, we used cultured mouse cortical collecting duct cells to see how overexpression or silencing of epithelial sodium channel (ENaC) subunits and claudin-8 affect paracellular permeability. We also used conditional kidney tubule–specific knockout mice lacking ENaC subunits to assess the ENaC’s effect on claudin-8 expression.ResultsOverexpression or silencing of the ENaC γ-subunit was associated with parallel and specific changes in claudin-8 abundance. Increased claudin-8 abundance was associated with a reduction in paracellular permeability to sodium, whereas decreased claudin-8 abundance was associated with the opposite effect. Claudin-8 overexpression and silencing reproduced these functional effects on paracellular ion permeability. Conditional kidney tubule–specific ENaC γ-subunit knockout mice displayed decreased claudin-8 expression, confirming the cell culture experiments' findings. Importantly, ENaC β-subunit or α-subunit silencing or kidney tubule–specific β-ENaC or α-ENaC knockout mice did not alter claudin-8 abundance.ConclusionsOur data reveal the specific coupling between ENaC γ-subunit and claudin-8 expression. This coupling may play an important role in preventing the backflow of reabsorbed solutes and water to the tubular lumen, as well as in coupling paracellular and transcellular sodium permeability.

scholarly journals Grouper tshβ Promoter-Driven Transgenic Zebrafish Marks Proximal Kidney Tubule Development

PLoS ONE ◽  
2014 ◽  
Vol 9 (6) ◽  
pp. e97806 ◽  
Author(s):  
Yang Wang ◽  
Zhi-Hui Sun ◽  
Li Zhou ◽  
Zhi Li ◽  
Jian-Fang Gui
Keyword(s):  
Transgenic Zebrafish ◽  
Kidney Tubule ◽  
Proximal Kidney Tubule

Nondipping Blood Pressure: Predictive or Reactive Failure of Renal Sodium Handling?

Physiology ◽  
2021 ◽  
Vol 36 (1) ◽  
pp. 21-34 ◽  
Author(s):  
Jessica R. Ivy ◽  
Matthew A. Bailey
Keyword(s):  
Blood Pressure ◽  
Pressure Control ◽  
Sodium Reabsorption ◽  
Nocturnal Sleep ◽  
Sodium Homeostasis ◽  
Increased Risk ◽  
Health And Disease ◽  
Renal Sodium Handling ◽  
Sodium Handling

Blood pressure follows a daily rhythm, dipping during nocturnal sleep in humans. Attenuation of this dip (nondipping) is associated with increased risk of cardiovascular disease. Renal control of sodium homeostasis is essential for long-term blood pressure control. Sodium reabsorption and excretion have rhythms that rely on predictive/circadian as well as reactive adaptations. We explore how these rhythms might contribute to blood pressure rhythm in health and disease.

scholarly journals Fetal Undernutrition Programming, Sympathetic Nerve Activity, and Arterial Hypertension Development

2021 ◽  
Vol 12 ◽  
Author(s):  
Vinícius Schiavinatto Mariano ◽  
Patrícia Aline Boer ◽  
José Antônio Rocha Gontijo
Keyword(s):  
Blood Pressure ◽  
Arterial Hypertension ◽  
Protein Intake ◽  
Pressure Control ◽  
Sodium Reabsorption ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Functional Studies ◽  
Low Protein ◽  
Hypertension Development

A wealth of evidence showed that low birth weight is associated with environmental disruption during gestation, triggering embryotic or fetal adaptations and increasing the susceptibility of progeny to non-communicable diseases, including metabolic and cardiovascular diseases, obesity, and arterial hypertension. In addition, dietary disturbance during pregnancy in animal models has highlighted mechanisms that involve the genesis of arterial hypertension, particularly severe maternal low-protein intake (LP). Functional studies demonstrated that maternal low-protein intake leads to the renal decrease of sodium excretion and the dysfunction of the renin-angiotensin-aldosterone system signaling of LP offspring. The antinatriuretic effect is accentuated by a reduced number of nephron units and glomerulosclerosis, which are critical in establishing arterial hypertension phenotype. Also, in this way, studies have shown that the overactivity of the central and peripheral sympathetic nervous system occurs due to reduced sensory (afferent) renal nerve activity. As a result of this reciprocal and abnormal renorenal reflex, there is an enhanced tubule sodium proximal sodium reabsorption, which, at least in part, contributes directly to arterial hypertension development in some of the programmed models. A recent study has observed that significant changes in adrenal medulla secretion could be involved in the pathophysiological process of increasing blood pressure. Thus, this review aims to compile studies that link the central and peripheral sympathetic system activity mechanisms on water and salt handle and blood pressure control in the maternal protein-restricted offspring. Besides, these pathophysiological mechanisms mainly may involve the modulation of neurokinins and catecholamines pathways.

scholarly journals Endogenous Activation of Glucagon-Like Peptide-1 Receptor Contributes to Blood Pressure Control

Hypertension ◽  
2020 ◽  
Vol 76 (3) ◽  
pp. 839-848
Author(s):  
Flavia L. Martins ◽  
Matthew A. Bailey ◽  
Adriana C.C. Girardi
Keyword(s):  
Blood Pressure ◽  
Proximal Tubule ◽  
Wistar Rats ◽  
Renin Angiotensin System ◽  
Pressure Control ◽  
Sodium Reabsorption ◽  
Ang Ii ◽  
Relevant Effect ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

The pharmacological administration of GLP-1R (glucagon-like peptide-1 receptor) agonists reduces blood pressure (BP) in type 2 diabetes mellitus and nondiabetic patients. This study tested the hypothesis that endogenous GLP-1R signaling influences the regulation of BP. To this end, SHRs (spontaneously hypertensive rats) and Wistar rats were treated with the GLP-1R antagonist Ex9 (exendin-9) or vehicle for 4 weeks. Rats receiving the GLP-1R agonist Ex4 (exenatide) were used as an additional control. We found that blockade of baseline GLP-1R signaling by Ex9 increased systolic BP in both SHR and Wistar rats, compared with vehicle-treated animals, while Ex4 only reduced systolic BP in SHR. Higher systolic BP induced by Ex9 was accompanied by reduced lithium clearance and lower levels of NHE3 (Na + /H + exchanger isoform 3) phosphorylation at the serine 552, indicative of increased proximal tubule sodium reabsorption. Additionally, urinary AGT (angiotensinogen) and renal cortical concentration of Ang II (angiotensin II) were enhanced by Ex9. Conversely, Ex4 decreased both urinary AGT and cortical Ang II but exclusively in SHRs. Moreover, both SHR and Wistar rats treated with Ex9 displayed hyperinsulinemia as compared with vehicle-treated rats, whereas Ex4 reduced fasting insulin concentration in SHR. Collectively, these results suggest that endogenous GLP-1R signaling exerts a physiologically relevant effect on BP control, which may be attributable, in part, to its tonic actions on the proximal tubule NHE3-mediated sodium reabsorption, intrarenal renin-angiotensin system, and insulin sensitivity. The possible role of impaired GLP-1R signaling in the pathogenesis of hypertension warrants further investigation.

Mechanisms of the ifosfamide-induced inhibition of endocytosis in the rat proximal kidney tubule

2008 ◽  
Vol 82 (9) ◽  
pp. 607-614 ◽  
Author(s):  
Zeinab Yaseen ◽  
Christian Michoudet ◽  
Gabriel Baverel ◽  
Laurence Dubourg
Keyword(s):  
Kidney Tubule ◽  
Proximal Kidney Tubule
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