Adrenomedullin Stimulates Renin Release and Renin mRNA in Mouse Juxtaglomerular Granular Cells

Hypertension ◽  
1997 ◽  
Vol 29 (5) ◽  
pp. 1148-1155 ◽  
Author(s):  
Boye L. Jensen ◽  
Bernhard K. Krämer ◽  
Armin Kurtz
Keyword(s):  
Renin Release ◽  
Granular Cells ◽  
Renin Mrna

scholarly journals Cyclic AMP selectively increases renin mRNA stability in cultured juxtaglomerular granular cells.

1993 ◽  
Vol 268 (32) ◽  
pp. 24138-24144
Author(s):  
M Chen ◽  
J Schnermann ◽  
A.M. Smart ◽  
F.C. Brosius ◽  
P.D. Killen ◽  
...  
Keyword(s):  
Cyclic Amp ◽  
Mrna Stability ◽  
Granular Cells ◽  
Renin Mrna

scholarly journals Regulated renin release from 3T3-L1 adipocytes

2009 ◽  
Vol 296 (6) ◽  
pp. E1383-E1391 ◽  
Author(s):  
Jason D. Fowler ◽  
Nathan D. Johnson ◽  
Thomas A. Haroldson ◽  
Joy A. Brintnall ◽  
Julio E. Herrera ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Renin Angiotensin System ◽  
Fold Increase ◽  
Renin Release ◽  
Epididymal Adipose Tissue ◽  
Prostaglandin E ◽  
Mrna Levels ◽  
Angiotensin System ◽  
Renin Mrna ◽  
Obese Male

Whereas adipose tissue possesses a local renin-angiotensin system, the synthesis and regulated release of renin has not been addressed. To that end, we utilized differentiating 3T3-L1 cells and analyzed renin expression and secretion. Renin mRNA expression and protein enzymatic activity were not detectable in preadipocytes. However, upon differentiation, renin mRNA and both intracellular and extracellular renin activity were upregulated. In differentiated adipocytes, forskolin treatment resulted in a 28-fold increase in renin mRNA, whereas TNFα treatment decreased renin mRNA fourfold. IL-6, insulin, and angiotensin (Ang) II were without effect. In contrast, forskolin and TNFα each increased renin protein secretion 12- and sevenfold, respectively. Although both forskolin and TNFα induce lipolysis in adipocytes, fatty acids, prostaglandin E2, and lipopolysaccharide had no effect on renin mRNA or secretion. To evaluate the mechanism(s) by which forskolin and/or TNFα are able to regulate renin secretion, a general lipase inhibitor (E600) and PKA inhibitor (H89) were used. Both inhibitors attenuated forskolin-induced renin release, whereas they had no effect on TNFα-regulated secretion. In contrast, E600 potentiated forskolin-stimulated renin mRNA levels, whereas H89 had no effect. Neither inhibitor had any influence on TNFα regulation of renin mRNA. Relative to lean controls, renin expression was reduced 78% in the epididymal adipose tissue of obese male C57Bl/6J mice, consistent with TNFα-mediated downregulation of renin mRNA in the culture system. In conclusion, the expression and secretion of renin are regulated under a complex series of hormonal and metabolic determinants in mature 3T3-L1 adipocytes.

Real-time imaging of renin release in vitro

2004 ◽  
Vol 287 (2) ◽  
pp. F329-F335 ◽  
Author(s):  
János Peti-Peterdi ◽  
Attila Fintha ◽  
Amanda L. Fuson ◽  
Albert Tousson ◽  
Robert H. Chow
Keyword(s):  
Resonance Energy Transfer ◽  
Resonance Energy ◽  
Renin Angiotensin System ◽  
Granular Cell ◽  
Time Lapse ◽  
Renin Release ◽  
Granular Cells ◽  
Renin Substrate ◽  
Quinacrine Fluorescence

Renin release from juxtaglomerular granular cells is considered the rate-limiting step in activation of the renin-angiotensin system that helps to maintain body salt and water balance. Available assays to measure renin release are complex, indirect, and work with significant internal errors. To directly visualize and study the dynamics of both the release and tissue activity of renin, we isolated and perfused afferent arterioles with attached glomeruli dissected from rabbit kidneys and used multiphoton fluorescence imaging. Acidotropic fluorophores, such as quinacrine and LysoTrackers, clearly and selectively labeled renin granules. Immunohistochemistry of mouse kidney with a specific renin antibody and quinacrine staining colocalized renin granules and quinacrine fluorescence. A low-salt diet for 1 wk caused an approximately fivefold increase in the number of both individual granules and renin-positive granular cells. Time-lapse imaging showed no signs of granule trafficking or any movement, only the dimming and disappearance of fluorescence from individual renin granules within 1 s in response to 100 μM isoproterenol. There appeared to be a quantal release of the granular contents; i.e., an all-or-none phenomenon. Using As4.1 cells, a granular cell line, we observed further classic signs of granule exocytosis, the emptying of granule content associated with a flash of quinacrine fluorescence. Using a fluorescence resonance energy transfer-based, 5-(2-aminoethylamino)naphthalene-1-sulfonic acid (EDANS)-conjugated renin substrate in the bath, an increase in EDANS fluorescence (renin activity) was observed around granular cells in response to isoproterenol. Fluorescence microscopy is an excellent tool for the further study of the mechanism, regulation, and dynamics of renin release.

Renin expression in COX-2-knockout mice on normal or low-salt diets

2000 ◽  
Vol 279 (5) ◽  
pp. F819-F825 ◽  
Author(s):  
Tianxin Yang ◽  
Yoshimi Endo ◽  
Yuning G. Huang ◽  
Ann Smart ◽  
Josie P. Briggs ◽  
...  
Keyword(s):  
Knockout Mice ◽  
Contact Region ◽  
Contact Point ◽  
Renin Activity ◽  
Mrna Levels ◽  
Granular Cells ◽  
Wild Type ◽  
Low Salt ◽  
Renin Mrna ◽  
Cox 2

Experiments were performed in mice to investigate whether cyclooxygenase-2 (COX-2) in epithelial cells near the tubulovascular contact point (macula densa and TAL cells) may regulate renin gene expression in juxtaglomerular granular cells. Renin activity, afferent arteriolar granularity, and renin mRNA were determined in wild-type mice and in COX-2-knockout mice on control and low-NaCl diets. Renin activity in microdissected glomeruli assessed as angiotensin I formation in the presence of excess substrate and afferent arteriolar granularity determined by direct visualization and immunostaining were significantly reduced in COX-2 −/− compared with wild-type animals. Similarly, renal cortical mRNA levels were lower in COX-2 −/− than in wild-type mice. Maintaining mice on a low-salt diet for 14 days induced an increase in renin mRNA, afferent arteriolar granularity, and renin activity in wild-type mice. In contrast, renin mRNA and renin granularity did not significantly increase in low-salt-treated COX-2 −/− mice, whereas the increase in juxtaglomerular renin enzyme activity was markedly attenuated, but not fully blocked. In additional experiments we found that COX-2 mRNA was increased in angiotensin type 1A receptor-knockout mice compared with wild-type mice. We conclude that COX-2 in the tubulovascular contact region is a critical determinant of renin synthesis in granular cells under resting conditions and that it participates in the stimulation of renin expression caused by a low-NaCl intake.

Effect of nitric oxide on renin secretion. I. Studies in isolated juxtaglomerular granular cells

1995 ◽  
Vol 268 (5) ◽  
pp. F948-F952 ◽  
Author(s):  
S. G. Greenberg ◽  
X. R. He ◽  
J. B. Schnermann ◽  
J. P. Briggs
Keyword(s):  
Phosphodiesterase Inhibitor ◽  
Renin Secretion ◽  
Renin Release ◽  
Granular Cells ◽  
Short Term ◽  
Time Intervals ◽  
Superfusion System ◽  
A Cell ◽  
Short Time ◽  
Observation Period

Experiments were performed on juxtaglomerular granular cells (JGC) in short-term primary culture to determine the direct immediate effect of NO on renin secretion and to test whether JGC are able to generate NO. Renin secretion was measured repeatedly over short time intervals in a cell superfusion system. Renin release did not significantly decrease over a 40-min observation period in untreated JGC. Addition of sodium nitroprusside (SNP) caused a reduction in renin release (measured in nano-Goldblatt hog units vs. time, i.e., nGU/min) from 479 +/- 25, 423 +/- 70, and 388 +/- 54 nGU/min to 295 +/- 19 (n = 5), 102 +/- 21 (n = 7), and 71 +/- 9 nGU/min (n = 6) with 10(-5), 10(-4), and 10(-3) M SNP, respectively. In the presence of the guanylate cyclase inhibitor methylene blue at 10(-4) M, SNP at 10(-4) M had no significant effect on renin secretion. 8-Bromoguanosine 3',5'-cyclic monophosphate at 10(-4) M in the presence of the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (10(-3) M) caused a reduction of renin secretion to 50.1 +/- 3.6% of control. To examine the possibility that renin secretion is affected by NO release from JGC, we assessed the effect of the NO synthase (NOS) substrate L-arginine (10(-3) M) and the NOS blocker N omega-nitro-L-arginine (10(-4) M) on renin secretion. Renin release was not significantly altered by either stimulation or inhibition of NOS activity.(ABSTRACT TRUNCATED AT 250 WORDS)

The Renin–Angiotensin System in Newborn Dogs

1971 ◽  
Vol 49 (2) ◽  
pp. 134-138 ◽  
Author(s):  
P. Granger ◽  
J. M. Rojo-Ortega ◽  
S. Casado Pérez ◽  
R. Boucher ◽  
J. Genest
Keyword(s):  
Peritoneal Dialysis ◽  
Plasma Renin Activity ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Renin Activity ◽  
Renin Release ◽  
Granular Cells ◽  
Angiotensin System ◽  
Juxtaglomerular Cell ◽  
Detailed Evaluation

A detailed evaluation of the rennin–angiotensin system by concurrent determinations of plasma renin activity, renal renin activity, and juxtaglomerular index in newborn dogs during the first 15 days of extrauterine life is described. Findings show that the plasma renin activity is significantly higher for the first 2 weeks of extrauterine life when compared with the values found in adult dogs, and that the renal renin activity is slightly greater despite a very low juxtaglomerular index with a few granular cells, mostly located in the juxtamedullary cortex. Stimulation (peritoneal dialysis) of renin release resulted in a marked increase in plasma renin activity. The juxtaglomerular index was not modified by the stimulation whereas the renal renin activity decreased slightly. From these results, it is suggested that the formation and secretion of renin is well developed in kidneys of newborn dogs despite the absence of demonstrable juxtaglomerular cell granules.

Prostaglandins stimulate renin secretion and renin mRNA in mouse renal juxtaglomerular cells

1996 ◽  
Vol 271 (3) ◽  
pp. F659-F669 ◽  
Author(s):  
B. L. Jensen ◽  
C. Schmid ◽  
A. Kurtz
Keyword(s):  
Mesangial Cells ◽  
Direct Interaction ◽  
Granular Cell ◽  
Renin Secretion ◽  
Juxtaglomerular Cells ◽  
Granular Cells ◽  
Mrna Accumulation ◽  
Renin Mrna ◽  
Significant Expression ◽  
Dose Dependent

This study examined 1) effects of prostaglandins (PG) on renin secretion and renin gene expression from isolated juxtaglomerular granular cells and 2) expression of cyclooxygenases in juxtaglomerular structures. Incubation of granular cell cultures with PGE2, -I2, -F2 alpha, and thromboxane B2 identified PGI2 and PGE2 as stimulators of renin secretion; the effects were dose and time dependent. PGE2 also increased renin mRNA accumulation time and dose dependent. PGE2 and PGI2 activated adenylate cyclase concentration dependent in granular cells. PGE2 stimulations of renin secretion and renin mRNA were nonadditive to those of forskolin and were inhibited by endothelin. The findings are compatible with cellular actions through adenosine 3',5'-cyclic monophosphate (cAMP). On total RNA harvested from whole kidneys, from microdisected glomeruli with attached afferent arterioles and from mesangial cells in primary culture, reverse transcription-polymerase chain reaction revealed significant expression of cyclooxygenase I and II. By direct interaction with PG receptors on renal juxtaglomerular cells, PGE2 and PGI2 can act as potent and rapid stimulators of renin secretion and renin mRNA probably through cAMP-dependent pathways.

The structure of the gills of the axolotl, Ambystoma mexicanum

1987 ◽  
Vol 45 ◽  
pp. 824-825
Author(s):  
Mohinder S. Jarial
Keyword(s):  
Leydig Cells ◽  
Secretory Granules ◽  
Light And Electron Microscopy ◽  
Cell Types ◽  
Ambystoma Mexicanum ◽  
Basal Cells ◽  
Granular Cells ◽  
Gill Filaments ◽  
Mitotic Figures ◽  
Apical Membranes

The axolotl is a strictly aquatic salamander in which the larval external gills are retained throughout life. The external gills of the adult axolotl have been studied by light and electron microscopy for ultrastructural evidence of ionic transport. The thin epidermis of the gill filaments and gill stems is composed of 3 cell types: granular cells, the basal cells and a sparce population of intervening Leydig cells. The gill epidermis is devoid of muscles, and no mitotic figures were observed in any of its cells.The granular cells cover the gill surface as a continuous layer (Fig. 1, G) and contain secretory granules of different forms, located apically (Figs.1, 2, SG). Some granules are found intimately associated with the apical membrane while others fuse with it and release their contents onto the external surface (Fig. 3). The apical membranes of the granular cells exhibit microvilli which are covered by a PAS+ fuzzy coat, termed “glycocalyx” (Fig. 2, MV).

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