A new channel for the control of renin secretion in juxtaglomerular cells

2020 ◽  
Vol 98 (3) ◽  
pp. 543-545
Author(s):  
Francois Alhenc-Gelas
Keyword(s):  
Renin Secretion ◽  
Juxtaglomerular Cells

Renin secretion from permeabilized juxtaglomerular cells requires a permeant cation

1999 ◽  
Vol 437 (3) ◽  
pp. 449-454 ◽  
Author(s):  
Boye L. Jensen ◽  
Peter Ellekvist ◽  
O. Skøtt
Keyword(s):  
Renin Secretion ◽  
Juxtaglomerular Cells

Do Calcium-Activated Chloride Channels Control Renin Secretion?

Physiology ◽  
1990 ◽  
Vol 5 (2) ◽  
pp. 43-46 ◽  
Author(s):  
A Kurtz
Keyword(s):  
Chloride Channels ◽  
Renin Secretion ◽  
Volume Control ◽  
Juxtaglomerular Cells ◽  
Epithelioid Cells ◽  
Intracellular Ca ◽  
Cl Channels

The rate of renin secretion from renal juxtaglomerular epithelioid cells appears to be inversely correlated to intracellular Ca activity. Such a dependency of renin secretion on Ca activity could be controlled by Ca-activated Cl channels that may be involved in the volume control of juxtaglomerular cells.

Calcium in the control of renin secretion: Ca2+ influx as an inhibitory signal

1981 ◽  
Vol 240 (1) ◽  
pp. F70-F74 ◽  
Author(s):  
C. S. Park ◽  
D. S. Han ◽  
J. C. Fray
Keyword(s):  
Incubation Temperature ◽  
Inhibitory Effect ◽  
Renin Secretion ◽  
Juxtaglomerular Cells ◽  
Stimulatory Action ◽  
Inhibitory Signal ◽  
Ca Antagonist ◽  
K Concentration ◽  
Energy Dependent

The mechanism for the inhibition of renin secretion in vitro from renal cortical slices by angiotensin II, antidiuretic hormone, ouabain, and high K+ concentration was studied. The inhibitory effect of these agents was blocked by a Ca antagonist, verapamil. In addition, epinephrine stimulated renin secretion and its stimulatory action was blocked by ouabain. These results support the hypothesis that Ca2+ influx into juxtaglomerular cells plays a role as an inhibitory signal whereas Ca2+ efflux is a stimulatory signal for renin secretion. Renin secretion was greatly stimulated by lowering incubation temperature, indicating that renin secretion is not energy dependent. The possibility is discussed that Ca2+ of juxtaglomerular cells might activate an enzyme(s) that then modulates some sequential steps of renin secretory processes, thereby controlling the rate of renin secretion.

Regulation of in vitro renin secretion by ANG II feedback manipulation in vivo in the ovine fetus

1999 ◽  
Vol 277 (4) ◽  
pp. R1230-R1238 ◽  
Author(s):  
Carlos E. Giammattei ◽  
Jack W. Strandhoy ◽  
James C. Rose
Keyword(s):  
Feedback Regulation ◽  
Late Gestation ◽  
Renin Secretion ◽  
Juxtaglomerular Cells ◽  
Fetal Life ◽  
Ang Ii ◽  
Active Renin ◽  
Age Related

The renin-angiotensin system is critically important to fetal cardiovascular function and organ development. The feedback regulation of renin secretion by ANG II develops early in gestation yet does not linearly progress from fetal life to adulthood. Renin secretion is elevated in late gestation compared with earlier or postnatal time periods, which suggests that some component of the negative feedback regulation of renin secretion is less sensitive in late gestation. We examined in fetal sheep the age-related consequence of chronic in vivo manipulation of ANG II on renal renin secretion measured in vitro. Immature (101–103 days of gestation) and mature (130–133 days of gestation) fetuses were treated for 72 h with enalaprilat, ANG II or vehicle. Content and basal and isoproterenol-stimulated secretion of prorenin (PR) and active renin (AR) from fetal kidney cortical slices were determined. Enalaprilat pretreatment in vivo increased renal renin content and basal and stimulated secretion of PR and AR in vitro even in immature animals. Immunohistochemical localization showed that enalaprilat treatment caused an age-related recruitment of renin-containing juxtaglomerular cells. Conversely, ANG II pretreatment decreased basal and stimulated PR and AR secretion from immature fetal kidneys, but only inhibited PR secretion from mature kidneys. It also caused an age-related decrease in the percentage of renin-containing juxtaglomerular cells. These results suggest that ANG II feedback modulates not only the synthesis and content of renin, but the sensitivity of the coupling between stimulus and secretion. A critical observation of our study is that the higher renal tissue concentrations of prorenin and active renin in late gestation may be a consequence of reduced sensitivity to ANG II feedback; this is consistent with the increased plasma concentrations of renin found in near-term mammals.

Do osmotic forces play a role in renin secretion?

1988 ◽  
Vol 255 (1) ◽  
pp. F1-F10 ◽  
Author(s):  
O. Skott
Keyword(s):  
Secretory Granules ◽  
Proton Gradient ◽  
Renin Secretion ◽  
Renin Release ◽  
Juxtaglomerular Cells ◽  
Proton Gradients ◽  
Low Calcium ◽  
Release In Vitro

Secretory granules swell during exocytosis. Swelling may follow fusion and assist in extrusion of the granular content, or swelling may cause granular fusion with the plasmalemma. A granular proton gradient has been suggested to be involved in such preexocytic granular swelling. Exocytosis of renin from juxtaglomerular cells of isolated preparations is very sensitive to changes in the extracellular osmolality. Extracellular hyposmolality causes swelling of secretory granules, fusions between peripherally located granules and plasmalemma, and an increased number of release episodes. Induction of granule swelling at constant extracellular osmolality also stimulates renin release. Newly recruited renin granules are osmosensitive, and a high extracellular osmolality blocks secretion induced by other means (low calcium). Dissipation of granular proton gradients inhibits renin release without affecting the osmosensitivity. Thus, in renin release in vitro, a granular swelling precedes fusion and exocytosis, and a granular proton gradient may contribute to preexocytic swelling when extracellular osmolality is constant. The osmosensitivity may be important for macula densamediated renin release.

Regulation of Renin Secretion and Renin Synthesis by Second Messengers in Isolated Mouse Juxtaglomerular Cells

1991 ◽  
Vol 1 (2) ◽  
pp. 98-110 ◽  
Author(s):  
Roberto Delia Bruna ◽  
Florence Pinet ◽  
Pierre Corvol ◽  
Armin Kurtz
Keyword(s):  
Second Messengers ◽  
Renin Secretion ◽  
Juxtaglomerular Cells ◽  
Renin Synthesis

scholarly journals Analysis of the calcium paradox of renin secretion

2018 ◽  
Vol 315 (4) ◽  
pp. F834-F843 ◽  
Author(s):  
D. Steppan ◽  
L. Pan ◽  
K. W. Gross ◽  
A. Kurtz
Keyword(s):  
Light Chain ◽  
Myosin Light Chain ◽  
Calcium Concentration ◽  
Inhibitory Effect ◽  
Extracellular Calcium ◽  
Renin Secretion ◽  
Calcium Handling ◽  
Juxtaglomerular Cells ◽  
Extracellular Calcium Concentration ◽  
Electron Microscopical

The secretion of the protease renin from renal juxtaglomerular cells is enhanced by subnormal extracellular calcium concentrations. The mechanisms underlying this atypical effect of calcium have not yet been unraveled. We therefore aimed to characterize the effect of extracellular calcium concentration on calcium handling of juxtaglomerular cells and on renin secretion in more detail. For this purpose, we used a combination of experiments with isolated perfused mouse kidneys and direct calcium measurements in renin-secreting cells in situ. We found that lowering of the extracellular calcium concentration led to a sustained elevation of renin secretion. Electron-microscopical analysis of renin-secreting cells exposed to subnormal extracellular calcium concentrations revealed big omega-shaped structures resulting from the intracellular fusion and subsequent emptying of renin storage vesicles. The calcium concentration dependencies as well as the kinetics of changes were rather similar for renin secretion and for renovascular resistance. Since vascular resistance is fundamentally influenced by myosin light chain kinase (MLCK), myosin light chain phosphatase (MLCP), and Rho-associated protein kinase (Rho-K) activities, we examined the effects of MLCK-, MLCP-, and Rho-K inhibitors on renin secretion. Only MLCK inhibition stimulated renin secretion. Conversely, inhibition of MCLP activity lowered perfusate flow and strongly inhibited renin secretion, which could not be reversed by lowering of the extracellular calcium concentration. Renin-secreting cells and smooth muscle cells of afferent arterioles showed immunoreactivity of MLCK. These findings suggest that the inhibitory effect of calcium on renin secretion could be explained by phosphorylation-dependent processes under control of the MLCK.

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