scholarly journals Juxtaglomerular Apparatus

2020 ◽  
Author(s):  
Keyword(s):  
Juxtaglomerular Apparatus

The Juxtaglomerular Apparatus

1989 ◽  
Author(s):  
Roland Taugner ◽  
Eberhard Hackenthal
Keyword(s):  
Juxtaglomerular Apparatus

scholarly journals The Role of Serum Chloride in Acute and Chronic Heart Failure: A Narrative Review

2021 ◽  
Vol 11 (2) ◽  
pp. 87-98
Author(s):  
Frederick Berro Rivera ◽  
Pia Alfonso ◽  
Jem Marie Golbin ◽  
Kevin Lo ◽  
Edgar Lerma ◽  
...  
Keyword(s):  
Heart Failure ◽  
Chloride Channel ◽  
Chloride Channels ◽  
Prognostic Value ◽  
Diuretic Therapy ◽  
Juxtaglomerular Apparatus ◽  
Sodium Chloride Cotransporter ◽  
Serum Chloride ◽  
And Function

Clinical guidelines include diuretics for the treatment of heart failure (HF), not to decrease mortality but to decrease symptoms and hospitalizations. More attention has been paid to the worse outcomes, including mortality, associated with continual diuretic therapy due to hypochloremia. Studies have revealed a pivotal role for serum chloride in the pathophysiology of HF and is now a target of treatment to decrease mortality. The prognostic value of serum chloride in HF has been the subject of much attention. Mechanistically, the macula densa, a region in the renal juxtaglomerular apparatus, relies on chloride levels to sense salt and volume status. The recent discovery of with-no-lysine (K) (WNK) protein kinase as an intracellular chloride sensor sheds light on the possible reason of diuretic resistance in HF. The action of chloride on WNKs results in the upregulation of the sodium-potassium-chloride cotransporter and sodium-chloride cotransporter receptors, which could lead to increased electrolyte and fluid reabsorption. Genetic studies have revealed that a variant of a voltage-sensitive chloride channel (CLCNKA) gene leads to almost a 50% decrease in current amplitude and function of the renal chloride channel. This variant increases the risk of HF. Several trials exploring the prognostic value of chloride in both acute and chronic HF have shown mostly positive results, some even suggesting a stronger role than sodium. However, so far, interventional trials exploring serum chloride as a therapeutic target have been largely inconclusive. This study is a review of the pathophysiologic effects of hypochloremia in HF, the genetics of chloride channels, and clinical trials that are underway to investigate novel approaches to HF management.

Decrease in ambient [Cl-] stimulates nitric oxide release from cultured rat mesangial cells

1994 ◽  
Vol 267 (1) ◽  
pp. F190-F195 ◽  
Author(s):  
H. Tsukahara ◽  
Y. Krivenko ◽  
L. C. Moore ◽  
M. S. Goligorsky
Keyword(s):  
Nitric Oxide ◽  
Mesangial Cells ◽  
Ionic Composition ◽  
Juxtaglomerular Apparatus ◽  
Cytosolic Calcium ◽  
No Synthase ◽  
Tubuloglomerular Feedback ◽  
No Production ◽  
Rapid Reduction ◽  
No Release

It has been hypothesized that fluctuations of the ionic composition in the interstitium of juxtaglomerular apparatus (JGA) modulate the function of extraglomerular mesangial cells (MC), thereby participating in tubuloglomerular feedback (TGF) signal transmission. We examined the effects of isosmotic reductions in ambient sodium concentration ([Na+]) and [Cl-] on cytosolic calcium concentration ([Ca2+]i) in cultured rat MC. Rapid reduction of [Na+] or [Cl-] in the bath induced a concentration-dependent rise in [Ca2+]i. MC are much more sensitive to decreases in ambient [Cl-] than to [Na+]; a decrease in [Cl-] as small as 14 mM was sufficient to elicit a detectable [Ca2]i response. These observations suggest that MC can be readily stimulated by modest perturbations of extracellular [Cl-]. Next, we examined whether activation of MC by lowered ambient [Cl-] influences cellular nitric oxide (NO) production. Using an amperometric NO sensor, we found that a 13 mM decrease in ambient [Cl-] caused a rapid, Ca2+/calmodulin-dependent rise in NO release from MC. This response was not inhibitable by dexamethasone, indicating the involvement of the constitutive rather than the inducible type of NO synthase in MC. In addition, the NO release was blunted by indomethacin pretreatment, suggesting that a metabolite(s) of cyclooxygenase regulates the activation of NO synthase in MC. Our findings that small perturbations in external [Cl-] stimulate MC to release NO, a highly diffusible and rapidly acting vasodilator, provide a possible mechanism to explain the transmission of the signal for the TGF response within the JGA.

Expression of Transforming Growth Factor (β)3 in Hypertrophic Juxtaglomerular Apparatus

1994 ◽  
Vol 330 (1) ◽  
pp. 68-69 ◽  
Author(s):  
Patricio E. Ray ◽  
Bryan K. McCune ◽  
R. Ariel Gomez ◽  
Edward J. Ruley ◽  
Paul E. Klotman
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor ◽  
Juxtaglomerular Apparatus ◽  
Transforming Growth Factor Β

Increased transforming growth factor-β2 expression in the glomerular arteriole of the juxtaglomerular apparatus in a bartter's-like syndrome

1999 ◽  
Vol 30 (8) ◽  
pp. 992-995 ◽  
Author(s):  
Tatsuo Yamamoto ◽  
Tosiyuki Takahashi ◽  
Katsuhiko Yonemura ◽  
Katsuyuki Matsui ◽  
Mitsumasa Nagase ◽  
...  
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor ◽  
Juxtaglomerular Apparatus ◽  
Transforming Growth Factor Β2

Role of nitric oxide in the control of renin secretion

1998 ◽  
Vol 275 (6) ◽  
pp. F849-F862 ◽  
Author(s):  
Armin Kurtz ◽  
Charlotte Wagner
Keyword(s):  
Nitric Oxide ◽  
Kinase Activity ◽  
Constitutive Expression ◽  
Juxtaglomerular Apparatus ◽  
Renin Secretion ◽  
Protein Kinase Activity ◽  
Dependent Protein Kinase ◽  
Dependent Protein ◽  
Permissive Role

Because of the significant constitutive expression of NO synthases in the juxtaglomerular apparatus, nitric oxide (NO) is considered as a likely modulator of renin secretion. In most instances, NO appears as a tonic enhancer of renin secretion, acting via inhibition of cAMP degradation through the action of cGMP. Depending on as yet unknown factors, the stimulatory effect of NO on renin secretion may also switch to an inhibitory one that is compatible with the inhibition of renin secretion by cGMP-dependent protein kinase activity. Whether NO plays a direct regulatory role or a more permissive role in the control of renin secretion remains to be answered.

scholarly journals Herniation of the tuft with outgrowth of vessels through the glomerular entrance in diabetic nephropathy damages the juxtaglomerular apparatus

2019 ◽  
Vol 317 (2) ◽  
pp. F399-F410 ◽  
Author(s):  
Jana Löwen ◽  
Elisabeth Gröne ◽  
Hermann-Josef Gröne ◽  
Wilhelm Kriz
Keyword(s):  
Diabetic Nephropathy ◽  
Juxtaglomerular Apparatus ◽  
Tubuloglomerular Feedback ◽  
Mrna Levels ◽  
Vascular Endothelial ◽  
The Matrix ◽  
Matrix Expansion ◽  
Advanced Stages ◽  
Endothelial Growth Factor ◽  
Aberrant Vessels

As shown in our previous paper (Kriz W, Löwen J, Federico G, van den Born J, Gröne E, Gröne HJ. Am J Physiol Renal Physiol 312: F1101–F1111, 2017), mesangial matrix expansion in diabetic nephropathy (DN) results for a major part from the accumulation of worn-out undegraded glomerular basement membrane material. Here, based on the reevaluation of >900 biopsies of DN, we show that this process continues with the progression of the disease finally leading to the herniation of the matrix-overloaded tuft through the glomerular entrance to the outside. This leads to severe changes in the glomerular surroundings, including a dissociation of the juxtaglomerular apparatus with displacement of the macula densa. The herniation is associated with a prominent outgrowth of glomerular vessels from the tuft. Mostly, these aberrant vessels are an abnormal type of arteriole with frequent intramural insudations of plasma. They spread into glomerular surroundings extending in intertubular and periglomerular spaces. Their formation is associated with elevated mRNA levels of vascular endothelial growth factor-A, angiopoietins 1 and 2, and the corresponding receptors. Functionally, these processes seem to compromise tubuloglomerular feedback-related functions and may be one factor why Na+-glucose cotransporter-2 inhibitors are not effective in advanced stages of DN.

Upregulation of juxtaglomerular NOS1 and COX-2 precedes glomerulosclerosis in fawn-hooded hypertensive rats

2001 ◽  
Vol 280 (4) ◽  
pp. F706-F714 ◽  
Author(s):  
Wilko Weichert ◽  
Alexander Paliege ◽  
Abraham P. Provoost ◽  
Sebastian Bachmann
Keyword(s):  
Smooth Muscle Actin ◽  
Age Groups ◽  
Juxtaglomerular Apparatus ◽  
Thick Ascending Limb ◽  
Hypertensive Rats ◽  
Renin Mrna ◽  
The Media ◽  
Cox 2 ◽  
Nitric Oxide Synthase 1 ◽  
Oxide Synthase

This study describes elevated histochemical signals for nitric oxide synthase-1 (NOS1) and cyclooxygenase-2 (COX-2) in juxtaglomerular apparatus (JGA) and adjacent thick ascending limb of the kidney of fawn-hooded hypertensive rats (FHH). Two different age groups of FHH (8 and 16 wk; FHH8 and FHH16, respectively) were compared with genetically related fawn-hooded rats with normal blood pressure (FHL) that served as controls. Histopathological changes in FHH comprised focal segmental glomerulosclerosis (FSGS), focal matrix overexpression, and a moderate arteriolopathy with hypertrophy of the media, enhanced immunoreactivity for α-smooth muscle actin, and altered distribution of myofibrils. Macula densa NOS activity, as expressed by NADPH-diaphorase staining, and NOS1 mRNA abundance were significantly elevated in FHH8 (+153 and +88%; P < 0.05) and FHH16 (+93 and +98%; P < 0.05), respectively. Even higher elevations were registered for COX-2 immunoreactivity in FHH8 (+166%; P < 0.05) and FHH16 (+157%; P < 0.05). The intensity of renin immunoreactivity and renin mRNA expression in afferent arterioles was also elevated in FHH8 (+51 and +166%; P < 0.05) and FHH16 (+105 and +136%; P < 0.05), respectively. Thus we show that coordinate upregulation of tubular NOS1, COX-2, and renin expression precedes, and continues after, the manifestation of glomerulosclerotic damage in FHH. These observations may have implications in understanding the role of local paracrine mediators in glomerular disease.

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