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 Cellular control of renin secretion

1999 ◽  
Vol 202 (3) ◽  
pp. 219-225
Author(s):  
A. Kurtz ◽  
C. Wagner
Keyword(s):  
Protein Kinase ◽  
Inhibitory Action ◽  
Second Messengers ◽  
Present Knowledge ◽  
Renin Secretion ◽  
Protein Kinase G ◽  
Juxtaglomerular Cells ◽  
Kinase C ◽  
Cl Channels ◽  
Cellular Control

Renin secretion at the level of renal juxtaglomerular cells appears to be controlled mainly by classic second messengers such as Ca2+, cyclic AMP and cyclic GMP, which in turn exert their effects through oppositely acting protein kinases and probably also by affecting the activity of ion channels in the plasma membrane. Thus, protein kinase A stimulates renin secretion, whilst protein kinase C and protein kinase G II inhibit renin secretion. Moreover, Cl- channels could be involved in the mediation of the inhibitory action of Ca2+ on renin secretion. This review summarizes our present knowledge about the possible actions of these kinases in renal juxtaglomerular cells and considers pathways in the organ control of renin secretion.

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.

Aldosterone enhances renin gene expression in juxtaglomerular cells

2004 ◽  
Vol 286 (2) ◽  
pp. F349-F355 ◽  
Author(s):  
Jürgen Klar ◽  
Helga Vitzthum ◽  
Armin Kurtz
Keyword(s):  
Gene Expression ◽  
Primary Cultures ◽  
Cellular Level ◽  
Juxtaglomerular Cells ◽  
Mrna Levels ◽  
Renin Synthesis ◽  
Corticosteroid Hormones ◽  
Renin Gene ◽  
Renin Mrna ◽  
Mrna Half Life

The secretion and synthesis of renin as the key regulator of the renin-angiotensin-aldosterone system are directly controlled by ANG II in the sense of a negative feedback. Because we found that renal afferent arterioles including the juxtaglomerular portion express the mineralocorticoid receptor, we aimed to characterize a possible direct effect of aldosterone on renin synthesis and renin secretion at the level of renal juxtaglomerular cells. Aldosterone (100 nM) clearly enhanced renin mRNA levels in primary cultures of mouse juxtaglomerular cells prestimulated with isoproterenol (100 nM) but had no effect on the exocytosis of stored renin. Similarly, in the mouse juxtaglomerular cell line As4.1, aldosterone time and concentration dependently increased renin mRNA abundance and prorenin secretion up to 2.5-fold. Moreover, aldosterone potentiated cAMP-induced renin gene expression in As4.1 cells. The effect of aldosterone was inhibited by spironolactone and was mimicked by corticosteroid hormones but not by sex steroids. Aldosterone had no influence on basal renin promoter activity but increased the renin mRNA half-life about threefold. In summary, these data suggest that aldosterone exerts a direct positive effect on renin gene expression at the cellular level probably by stabilizing renin mRNA.

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.

Juxtaglomerular cells cultured on a reconstituted basement membrane

1992 ◽  
Vol 262 (3) ◽  
pp. C563-C568 ◽  
Author(s):  
B. M. Rayson
Keyword(s):  
Basement Membrane ◽  
Primary Cultures ◽  
T Antigen ◽  
Temperature Sensitive ◽  
Juxtaglomerular Cells ◽  
Cellular Mechanisms ◽  
Sv40 Large T Antigen ◽  
Renin Synthesis ◽  
First Time

Circulating renin levels are regulated by release from juxtaglomerular (JG) cells. Here, for the first time, we describe the primary culture of rat juxtaglomerular cells on a reconstituted basement membrane. In addition, primary cultures were transformed with a temperature-sensitive SV40 large T antigen gene to promote the development of a continuous JG cell line. Both primary cultures and transformed JG cells maintain a highly differentiated state and secrete active renin. These preparations now provide a system in which characterization of the cellular mechanisms of regulation of renin synthesis and release is possible.

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