scholarly journals Regulation of the Renal NaCl Cotransporter and Its Role in Potassium Homeostasis

2020 ◽  
Vol 100 (1) ◽  
pp. 321-356 ◽  
Author(s):  
Ewout J. Hoorn ◽  
Martin Gritter ◽  
Catherina A. Cuevas ◽  
Robert A. Fenton
Keyword(s):  
Renin Angiotensin System ◽  
Epidemiological Data ◽  
Feedback Mechanism ◽  
High K ◽  
Dietary Potassium ◽  
Health And Disease ◽  
Rapid Removal ◽  
Nacl Cotransporter ◽  
Salt Sensitive Hypertension ◽  
Low K

Daily dietary potassium (K+) intake may be as large as the extracellular K+ pool. To avoid acute hyperkalemia, rapid removal of K+ from the extracellular space is essential. This is achieved by translocating K+ into cells and increasing urinary K+ excretion. Emerging data now indicate that the renal thiazide-sensitive NaCl cotransporter (NCC) is critically involved in this homeostatic kaliuretic response. This suggests that the early distal convoluted tubule (DCT) is a K+ sensor that can modify sodium (Na+) delivery to downstream segments to promote or limit K+ secretion. K+ sensing is mediated by the basolateral K+ channels Kir4.1/5.1, a capacity that the DCT likely shares with other nephron segments. Thus, next to K+-induced aldosterone secretion, K+ sensing by renal epithelial cells represents a second feedback mechanism to control K+ balance. NCC’s role in K+ homeostasis has both physiological and pathophysiological implications. During hypovolemia, NCC activation by the renin-angiotensin system stimulates Na+ reabsorption while preventing K+ secretion. Conversely, NCC inactivation by high dietary K+ intake maximizes kaliuresis and limits Na+ retention, despite high aldosterone levels. NCC activation by a low-K+ diet contributes to salt-sensitive hypertension. K+-induced natriuresis through NCC offers a novel explanation for the antihypertensive effects of a high-K+ diet. A possible role for K+ in chronic kidney disease is also emerging, as epidemiological data reveal associations between higher urinary K+ excretion and improved renal outcomes. This comprehensive review will embed these novel insights on NCC regulation into existing concepts of K+ homeostasis in health and disease.

Electron Probe Analysis of Vertebrate Smooth Muscle: Distribution of Ca and Ci

1976 ◽  
Vol 34 ◽  
pp. 334-335 ◽  
Author(s):  
Avril V. Somlyo ◽  
H. Shuman ◽  
A.P. Somlyo
Keyword(s):  
Smooth Muscle ◽  
Electron Probe ◽  
Preliminary Report ◽  
Cell Damage ◽  
Electron Probe Analysis ◽  
Perinuclear Space ◽  
Probe Analysis ◽  
High K ◽  
Low K ◽  
Initial Results

This is a preliminary report of electron probe analysis of rabbit portal-anterior mesenteric vein (PAMV) smooth muscle cryosectioned without fixation or cryoprotection. The instrumentation and method of electron probe quantitation used (1) and our initial results with cardiac (2) and skeletal (3) muscle have been presented elsewhere.In preparations depolarized with high K (K2SO4) solution, significant calcium peaks were detected over the sarcoplasmic reticulum (Fig 1 and 2) and the continuous perinuclear space. In some of the fibers there were also significant (up to 200 mM/kg dry wt) calcium peaks over the mitochondria. However, in smooth muscle that was not depolarized, high mitochondrial Ca was found in fibers that also contained elevated Na and low K (Fig 3). Therefore, the possibility that these Ca-loaded mitochondria are indicative of cell damage remains to be ruled out.

High breakdown voltage AlGaN/GaN HEMT with high‐K/low‐K compound passivation

2015 ◽  
Vol 51 (1) ◽  
pp. 104-106 ◽  
Author(s):  
Jiangfeng Du ◽  
Nanting Chen ◽  
Peilin Pan ◽  
Zhiyuan Bai ◽  
Liang Li ◽  
...  
Keyword(s):  
Breakdown Voltage ◽  
Gan Hemt ◽  
High Breakdown Voltage ◽  
High K ◽  
Low K

Hypokalemia induces renal injury and alterations in vasoactive mediators that favor salt sensitivity

2001 ◽  
Vol 281 (4) ◽  
pp. F620-F629 ◽  
Author(s):  
Shin-Ichi Suga ◽  
M. Ian Phillips ◽  
Patricio E. Ray ◽  
James A. Raleigh ◽  
Carlos P. Vio ◽  
...  
Keyword(s):  
Renal Injury ◽  
Renin Angiotensin System ◽  
Salt Sensitivity ◽  
Prostaglandin E ◽  
Tubulointerstitial Injury ◽  
Angiotensin System ◽  
Vasoactive Mediators ◽  
Hypoxia Marker ◽  
Renal Kallikrein ◽  
Salt Sensitive Hypertension

We investigated the hypothesis that hypokalemia might induce renal injury via a mechanism that involves subtle renal injury and alterations in local vasoactive mediators that would favor sodium retention. To test this hypothesis, we conducted studies in rats with diet-induced K+deficiency. We also determined whether rats with hypokalemic nephropathy show salt sensitivity. Twelve weeks of hypokalemia resulted in a decrease in creatinine clearance, tubulointerstitial injury with macrophage infiltration, interstitial collagen type III deposition, and an increase in osteopontin expression (a tubular marker of injury). The renal injury was greatest in the outer medulla with radiation into the cortex, suggestive of an ischemic etiology. Consistent with this hypothesis, we found an increased uptake of a hypoxia marker, pimonidazole, in the cortex. The intrarenal injury was associated with increased cortical angiontensin-converting enzyme (ACE) expression and continued cortical angiotensin II generation despite systemic suppression of the renin-angiotensin system, an increase in renal endothelin-1, a decrease in renal kallikrein, and a decrease in urinary nitrite/nitrates and prostaglandin E2 excretion. At 12 wk, hypokalemic rats were placed on a normal-K+ diet with either high (4%)- or low (0.01%)-NaCl content. Despite correction of hypokalemia and normalization of renal function, previously hypokalemic rats showed an elevated blood pressure in response to a high-salt diet compared with normokalemic controls. Hypokalemia is associated with alterations in vasoactive mediators that favor intrarenal vasoconstriction and an ischemic pattern of renal injury. These alterations may predispose the animals to salt-sensitive hypertension that manifests despite normalization of the serum K+.

Cardiac fibrillation in batrachia

1959 ◽  
Vol 197 (6) ◽  
pp. 1157-1160
Author(s):  
H. Mazzella
Keyword(s):  
Electric Shock ◽  
Opposite Effect ◽  
Mechanical Responses ◽  
T Wave ◽  
Mammalian Heart ◽  
Cardiac Fibrillation ◽  
High K ◽  
Bufo Arenarum ◽  
Low K ◽  
Toad Bufo

A study was made of fibrillation and its production in the heart of the toad ( Bufo arenarum). Application of a strong electric shock during the interval of the T wave, or just before, produced fibrillatory response in the ventricle. Repetitive stimuli were necessary for production of fibrillation in the auricle. Fibrillation was of a coarse type but at 37°C it occurred more readily and resembled more nearly that of the mammalian heart. At 5°C the opposite effect occurred. Perfusion of the heart with high K+ solution reduced vulnerability while in low K+ fibrillation occurred more readily. Absence of Ca++ shortened durations of induced fibrillations. Changes in mechanical responses were compared with changes in electrograms.

scholarly journals Neuronal (pro)renin receptor regulates deoxycorticosterone-induced sodium intake

2018 ◽  
Vol 50 (10) ◽  
pp. 904-912 ◽  
Author(s):  
Fatima Trebak ◽  
Wencheng Li ◽  
Yumei Feng
Keyword(s):  
Sodium Intake ◽  
Renin Angiotensin System ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
Sodium Balance ◽  
Total Fluid Intake ◽  
Sodium Deficiency ◽  
Sodium Appetite ◽  
The Central Nervous System ◽  
Salt Sensitive Hypertension

Increased sodium appetite is a physiological response to sodium deficiency; however, it has also been implicated in disease conditions such as congestive heart failure, kidney failure, and salt-sensitive hypertension. The central nervous system is the major regulator of sodium appetite and intake behavior; however, the neural mechanisms underlying this behavior remain incompletely understood. Here, we investigated the involvement of the (pro)renin receptor (PRR), a component of the brain renin-angiotensin system, in the regulation of sodium intake in a neuron-specific PRR knockout (PRRKO) mouse model generated previously in our laboratory. Sodium intake following deoxycorticosterone (DOCA) stimulation was tested by assessing the preference of mice for 0.9% saline or regular water in single-animal metabolic cages. Blood pressure was monitored in conscious, freely moving mice by a telemetry system. We found that saline intake and total fluid intake were significantly reduced in PRRKO mice following DOCA treatment compared with that in wild-type (WT) mice, whereas regular water intake was similar between the genotypes. Sodium preference and total sodium intake were significantly reduced in PRRKO mice compared with WT mice. PRRKO mice also excreted less urine and urinary sodium compared with WT mice following DOCA treatment, whereas potassium excretion was similar between the two groups. Finally, we found that the sodium balance, calculated by subtracting urinary sodium excretion from sodium intake, was greater in WT mice than in PRRKO mice. Collectively, these findings suggest that the neuronal PRR plays a regulatory role in DOCA-induced sodium intake.

Letter To The Editor

PEDIATRICS ◽  
1970 ◽  
Vol 46 (2) ◽  
pp. 317-317
Author(s):  
Jerome Liebman
Keyword(s):  
Control Theory ◽  
Renin Angiotensin System ◽  
Feedback Mechanism ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Letter To The Editor

Dr. Liebman writes as follows: Dr. Guntheroth's excellent comments are worth noting. Obviously, there are no data from our paper or anybody else's that give evidence that the renin-angiotensin system did not begin the chain of events ending in hypertension. Furthermore, the control theory-feedback mechanism concept for hypertension as expressed by Dr. Guyton indicate that renin levels should be normal at this time. However, other than the fact that it makes sense that the renin-angiotensin system started it all, what evidence is there that it did indeed start it all.

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