Renin Status of the Afferent Arteriole and Ultrastructure of the Juxtaglomerular Apparatus in ‘Superficial’ Juxtamedullary Nephrons from Rats

1986 ◽  
Vol 9 (6) ◽  
pp. 348-356
Author(s):  
Daniel Casellas ◽  
Roland Taugner
Keyword(s):  
Juxtaglomerular Apparatus ◽  
Afferent Arteriole

Immunocytochemical localization of renin in the developing ovine fetus

1996 ◽  
Vol 8 (1) ◽  
pp. 97 ◽  
Author(s):  
NM Rawashdeh ◽  
JC Rose ◽  
MS Rogers ◽  
C Giammattei ◽  
SS Iskandar
Keyword(s):  
Plasma Renin ◽  
Juxtaglomerular Apparatus ◽  
Afferent Arteriole ◽  
Vascular Tree ◽  
Developmentally Regulated ◽  
Newborn Lamb ◽  
Adult Sheep ◽  
Ovine Fetus ◽  
Ovine Fetal ◽  
Renin Content

The ontogeny of renin distribution in the outer cortical segments was studied by immunocytochemistry in two groups of ovine fetal kidneys; one set of fetal kidneys was obtained at 104-106 days (0.73 gestation, n = 6), and the other at 138-140 days (0.96 gestation, n = 6). Similar studies were performed in kidneys obtained from a lamb (2 weeks old) and from non-pregnant adult sheep, n = 4. Using rabbit anti-mouse renin antiserum that was proven to cross react with sheep renin and 0.033% 3',3'-diamino benzidine tetrachloride as a chromogen, immunoreactivity was found to be localized in the classical juxtaglomerular apparatus and the afferent arteriole in the immature fetuses, newborn lamb and adult sheep. In the mature fetuses a more extensive distribution was noted. Immunoreactivity was found in the afferent arteriole and the juxtaglomerular apparatus as well as other segments of the arterial vascular tree. These findings suggest that renal renin distribution in the lamb fetus is developmentally regulated. The results also correlate well with reports about renal cortical renin content and plasma renin activity at the stages studied. These observations further support the hypothesis that increased renal renin expression occurs in the fetus just prior to birth.

Localization of kallikrein in the rat kidney and its anatomical relationship to renin.

1982 ◽  
Vol 30 (4) ◽  
pp. 385-390 ◽  
Author(s):  
T B Orstavvik ◽  
T Inagami
Keyword(s):  
Collecting Duct ◽  
Rat Kidney ◽  
Distal Tubule ◽  
Juxtaglomerular Apparatus ◽  
Thick Ascending Limb ◽  
Loop Of Henle ◽  
Afferent Arteriole ◽  
Epitheloid Cells ◽  
Anatomical Relationship

The anatomical relationship between kallikrein and renin in the rat kidney was investigated immunohistochemically by the peroxidase-antiperoxidase method. Kallikrein was localized to the convoluted distal tubule, starting at a point, distal to the juxtaglomerular apparatus, where the thick ascending limb of loop of Henle transformed into the convoluted distal tubule. The thick ascending limb was identified by its content of uromucoid (Tamm-Horsfall glycoprotein). Kallikrein was never observed within the juxtaglomerular apparatus itself. The kallikrein-containing tubule ended where the distal tubule submerged into the collecting duct. Renin was found in epitheloid cells of the afferent arteriole. When neighboring sections were stained for kallikrein and renin, respectively, no close anatomical relationship was observed between the kallikrein-containing and the renin-containing structures.

Phospholemman expression in extraglomerular mesangium and afferent arteriole of the juxtaglomerular apparatus

2003 ◽  
Vol 285 (1) ◽  
pp. F121-F129 ◽  
Author(s):  
Randall K. Wetzel ◽  
Kathleen J. Sweadner
Keyword(s):  
Blood Flow ◽  
Membrane Protein ◽  
Molecular Mechanisms ◽  
Juxtaglomerular Apparatus ◽  
Macula Densa ◽  
Tubuloglomerular Feedback ◽  
Afferent Arteriole ◽  
Γ Subunit ◽  
Goormaghtigh Cells

The molecular mechanisms with which the juxtaglomerular apparatus accomplishes its twin functions, acute regulation of glomerular blood flow and secretion of renin, are still not clearly understood. Least understood is the role of the extraglomerular mesangial (EM) cells, also known as lacis or Goormaghtigh cells, which lie sandwiched between the macula densa and the afferent and efferent arterioles. Here, we report that immunoreactivity for phospholemman (FXYD1), a single-span membrane protein homologous to the gamma (γ) sub-unit of the Na,K-ATPase, is found in the kidney in EM cells with the Na,K-ATPase β2-subunit and in cortical blood vessels and the afferent arteriole with Na,K-ATPase α2 and β2. Phospholemman's distribution in EM cells is distinct from that of the Na,K-ATPase γ-subunit, which is found on the basolateral surface of macula densa cells with Na,K-ATPase α1 and β1. Phospholemman is a major kinase target, and its location in the juxtaglomerular apparatus suggests that it is involved in tubuloglomerular feedback.

The Juxtaglomerular Apparatus

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

Afferent arteriolar diameter in DOCA-salt and two-kidney one-clip hypertensive rats

1983 ◽  
Vol 245 (6) ◽  
pp. F755-F762 ◽  
Author(s):  
B. M. Iversen ◽  
L. Morkrid ◽  
J. Ofstad
Keyword(s):  
Blood Pressure ◽  
Plasma Renin ◽  
Afferent Arteriole ◽  
Cortical Layers ◽  
Hypertensive Rats ◽  
Salt Hypertension ◽  
Nephron Loss ◽  
Microsphere Method ◽  
Arteriolar Diameter ◽  
Equal Thickness

The afferent arteriolar diameter (dAA) was investigated during development of hypertensive renal disease in normal and uninephrectomized control rats, in chronic DOCA-salt (DOCA), post-DOCA (p-DOCA), and chronic two-kidney one-clip (2K-1C) hypertensive rats, and in post-two-kidney one-clip (p-2K-1C) normotensive rats. dAA was measured by the microsphere method. Nephron loss was present in the kidneys exposed to elevate blood pressure. The dAA was reduced from 19.9 to 17.2 micron in the DOCA group (P less than 0.001) and from 19.1 to 16.3 micron in the nonclipped kidneys in the 2K-1C group (P less than 0.001). The dAA increased from 19.9 to 20.7 micron in the p-DOCA group. Afferent arteriolar dilatation from 19.1 to 21.0 micron (P less than 0.001) was present about 50 days after clipping in the 2K-1C group; in the clipped kidneys the dAA returned to normal (18.9 micron) after declipping. No relation between the dAA and plasma renin concentration was observed. In all models dAA was the same in three cortical layers of equal thickness. Accordingly, chronic renal DOCA-salt hypertension constricts the afferent arteriole with angiotensin-independent mechanisms. Autoregulatory dilatation of the afferent arteriole seems to be maintained for at least 50 days. When the hypertension is moderate, dAA in damaged kidneys may be dilated.

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
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