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.

Effects of endothelin on in vitro renin secretion

1991 ◽  
Vol 260 (4) ◽  
pp. E521-E525 ◽  
Author(s):  
O. Moe ◽  
A. Tejedor ◽  
W. B. Campbell ◽  
R. J. Alpern ◽  
W. L. Henrich
Keyword(s):  
Rat Kidney ◽  
Renin Secretion ◽  
Renin Release ◽  
Juxtaglomerular Cells ◽  
Tetraacetic Acid ◽  
Direct Effects ◽  
Calcium Buffer ◽  
Renin Inhibition ◽  
Cortical Slices

The ability of endothelin-1 (ET-1) to directly inhibit renal renin secretion in the presence of a renin stimulator is unknown, as is the mechanism of action of any renin inhibition. Thus direct effects of ET-1 on renin secretion were investigated in two distinct preparations: rat kidney cortical slices and isolated juxtaglomerular cells (JGC). In rat kidney cortical slices, ET-1 reduced basal renin release by 20 (P less than 0.05) and 44% (P less than 0.005) at 10(-9) and 10(-8) M, respectively. To test the efficacy of ET-1 as a renin inhibitor, experiments were performed in the presence of the renin stimulator isoproterenol (10(-5) M). Addition of isoproterenol to cortical slices increased renin release by 97% (P less than 0.001); ET-1 (10(-8) M) limited this increase in renin release by isoproterenol by 80% (P less than 0.05). Similar effects were observed in JGC as ET-1 (10(-8) M) significantly reduced basal renin secretion by 26% (P less than 0.05). In isolated JGC, isoproterenol increased renin secretion by 151% (P less than 0.001); ET-1 (10(-8) M) significantly reduced this stimulated increase in renin secretion by 68%. The mechanism of renin inhibition was examined by testing the effects of the intracellular calcium buffer 1,2-bis(2-aminophenoxy) ethane-N,N,N',N'-tetraacetic acid (BAPTA; 10(-6) M) in JGC. BAPTA alone increased renin secretion in JGC by 116% (P less than 0.01); when the combination of (10(-6) M) BAPTA and ET-1 (10(-8) M) were tested in the JGC, renin secretion still increased significantly (by 78%, P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Stimulatory action of parathyroid hormone on renin secretion in vitro: a study using isolated rat kidney, isolated rabbit glomeruli and superfused dispersed rat juxtaglomerular cells

1993 ◽  
Vol 84 (1) ◽  
pp. 11-19 ◽  
Author(s):  
Christian Saussine ◽  
C. Judes ◽  
T. Massfelder ◽  
M.-J. Musso ◽  
U. Simeoni ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Rat Kidney ◽  
Renin Secretion ◽  
Renin Release ◽  
Juxtaglomerular Cells ◽  
Isolated Kidney ◽  
Stimulatory Action ◽  
Isolated Rat Kidney ◽  
Isolated Rat

1. We have previously reported that pharmacological concentrations (125 nmol/l) of parathyroid hormone may stimulate renin release in the stable recirculating and non-filtering isolated rat kidney. 2. In the present study we have attempted to extend these initial observations by examining the concentration-related response of renin release to parathyroid hormone, using the same model of isolated kidney, and determining whether the effect of parathyroid hormone on renin release can be demonstrated by more direct approaches. Thus, the effects of parathyroid hormone on renin secretion were investigated in two other renal preparations: isolated rabbit glomeruli and isolated rat juxtaglomerular cells. 3. In the isolated kidney, rat parathyroid hormone significantly stimulated renin accumulation in the perfusate in a concentration-related manner with a threshold of 1 nmol/l. 4. In both glomeruli and juxtaglomerular cells bovine [Nle8,18,Tyr34]parathyroid hormone-(1–34)amide effectively and repeatedly stimulated renin release. These results imply that there is a direct stimulatory effect of parathyroid hormone on renin release. 5. We also examined the effect of [Nle8,18, Tyr34]parathyroid hormone-(l-34)amide during extracellular calcium buffering in the glomeruli. [Nle8,18,Tyr34]parathyroid hormone-(1–34)amide was uneffective in calcium-free medium. Increasing the extracellular ionized calcium concentration to 2.5 mmol/l increased the extent of stimulation in accordance with the reported ability of parathyroid hormone to block calcium channels and relax vascular smooth muscle cells. 6. These results provide further support for the role of parathyroid hormone as a direct mediator of renin secretion; moreover, the renin-stimulating action of parathyroid hormone may be mediated through the inhibition of calcium influx.s

Prostaglandins and renin release in vitro

1981 ◽  
Vol 240 (6) ◽  
pp. E609-E614
Author(s):  
C. S. Lin ◽  
H. Iwao ◽  
S. Puttkammer ◽  
A. M. Michelakis
Keyword(s):  
Arachidonic Acid ◽  
Renal Cortex ◽  
The Other ◽  
Renin Release ◽  
Eicosatetraenoic Acid ◽  
Juxtaglomerular Cells ◽  
Prostaglandin F2 Alpha ◽  
Prostaglandin System

The present studies were undertaken to explore further the role of prostaglandins in the release of renin from the renal cortex. To provide the best assessment of renin release, renin was determined by a radioimmunoassay for the direct measurement of renin. Slices of mouse renal cortex were incubated at 37 degrees C with arachidonic acid (AA), 5,8,11,14-eicosatetraenoic acid (ETA), indomethacin, prostaglandins, and synthetic prostaglandin endoperoxide analogue (EPA). Our results showed that AA at 1.5 X 10(-8) M significantly increased renin release at 10 and 30 min of incubation. This renin increase ws abolished by either ETA or indomethacin. Prostaglandin F2 alpha (PGF2 alpha) also significantly stimulated renin release at 10 and 60 min. PGE2 and 16,16-dimethyl PGE2 (DMPGE2) showed much less renin release-stimulating activity. EPA and PGI2 on the other hand very strongly stimulated renin release. However, at higher concentrations the stimulating effect of PGI2 and EPA disappeared and even became inhibitory in the case of EPA. Other prostaglandins were found to have no effect on renin release. The results suggest that the prostaglandin system directly affects renin release from the juxtaglomerular cells independent of systemic neurogenic and hemodynamic influences.

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.

Measurement of renin secretion in single perfused rabbit glomeruli

1990 ◽  
Vol 258 (5) ◽  
pp. F1460-F1465 ◽  
Author(s):  
H. A. Bock ◽  
M. Hermle ◽  
A. Fiallo ◽  
R. W. Osgood ◽  
T. A. Fried
Keyword(s):  
Perfusion Pressure ◽  
Secretion Rate ◽  
Renin Secretion ◽  
Renin Release ◽  
Afferent Arteriole ◽  
Adrenergic Nervous System ◽  
A New Technique ◽  
New Perspective ◽  
Bowman's Capsule

A new technique is presented that allows the measurement of the renin secretion rate of single rabbit glomeruli during in vitro perfusion at controlled afferent arteriolar perfusion pressure. Rabbit glomeruli with intact afferent arteriole and Bowman's capsule are obtained by microdissection and cannulated with a pipette system that allows continuous afferent arteriolar pressure measurement. The renin secretion rate of 10 glomeruli, perfused at 40 mmHg, was measured in 15-min intervals with an antibody-trapping microassay. Renin secretion rate was low relative to total renin content (1.2-2.0% of content/perfusion h) and increased three- to fivefold in response to isoproterenol (10(-5) M). The afferent arteriole contracted to norepinephrine (10(-5) M) in each instance. This novel, although difficult, technique allows the study of renin release in vitro at controlled perfusion pressure, without the interfering effects of the macula densa, arterial angiotensin II, and the adrenergic nervous system. It should allow a new perspective on issues such as the pressure-flow dependence of renin release and the interaction of the afferent arteriolar endothelium with the renin-secreting juxtaglomerular cells.

Osmotically sensitive renin release from permeabilized juxtaglomerular cells

1993 ◽  
Vol 265 (1) ◽  
pp. F87-F95 ◽  
Author(s):  
B. L. Jensen ◽  
O. Skott
Keyword(s):  
Secretory Granules ◽  
Sucrose Concentration ◽  
Proximal Tubules ◽  
Renin Release ◽  
Continuous Exposure ◽  
Juxtaglomerular Cells ◽  
Water Fluxes ◽  
Intact Cells ◽  
Permeabilized Cells ◽  
Cellular Volume

Renin secretion from juxtaglomerular (JG) cells is sensitive to external osmolality in a way that has been suggested to depend either on cellular volume or on effects on secretory granules. To distinguish between these possibilities, a technique for permeabilization of JG cell membranes was developed. Rat glomeruli with attached JG cells were isolated and permeabilized by 20 microM digitonin for 12 min and followed by continuous exposure to 2 microM digitonin. Experiments on proximal tubules showed that cellular volume was unaffected by changes in external sucrose concentration after a similar permeabilization procedure. With permeabilized JG cells the following changes in osmolality were tested (in mM sucrose): +90 (n = 6), +60 (n = 5), +30 (n = 6), +15 (n = 6), -15 (n = 5), -30 (n = 6), -60 (n = 6), and -90 (n = 6). With nonpermeabilized cells similar experiments were done with changes of +90 (n = 7), +30 (n = 4), -30 (n = 4), and -90 (n = 6) mM sucrose. Increases in osmolality caused inhibition of renin release, whereas decreases stimulated secretion. Within +/- 10% variations in osmolality there were no differences between the responses in permeabilized and intact cells, whereas the responses with larger changes were less in the permeabilized cells. Increase or decrease in urea concentration by 30 mM did not affect renin release. Thus water fluxes can influence renin release by a mechanism that is independent of cell volume.

RENIN SECRETION IN VITRO FROM RAT KIDNEY CORTEX SLICES

1969 ◽  
Vol 60 (3) ◽  
pp. 550-554 ◽  
Author(s):  
Lj. Božović ◽  
S. Efendić
Keyword(s):  
Rat Kidney ◽  
Renin Secretion ◽  
Renin Release ◽  
Kidney Cortex ◽  
Rat Kidney Cortex ◽  
Active Mechanism ◽  
Cortex Slices ◽  
Kidney Cortex Slices

ABSTRACT A method for in vitro studies of renin release is described. Kidney cortex slices taken from control rats and rats stimulated to release renin were incubated with and without glucose. Renin release from the slices to a large extent was glucose-dependent. This result supports the hypothesis of an active mechanism of renin secretion.

Inhibition of renin secretion from rat renal cortical slices by (R)-12-HETE

1992 ◽  
Vol 263 (4) ◽  
pp. F665-F670
Author(s):  
W. L. Henrich ◽  
J. R. Falck ◽  
W. B. Campbell
Keyword(s):  
High Performance ◽  
Enzyme System ◽  
Renin Secretion ◽  
Renin Release ◽  
Arachidonic Acid Metabolite ◽  
Chiral Phase ◽  
Cytochrome P 450 ◽  
Cortical Slices

The arachidonic acid metabolite 12-hydroxyeicosatetraenoic acid (12-HETE) inhibits renin secretion both in vivo and in vitro, but the enzymatic origin of the 12-HETE responsible for renin inhibition is unknown. These studies examined the effect of the 12-HETE stereoisomers (R)-12-HETE (a product of the cytochrome P-450 monooxygenase enzyme system) and (S)-12-HETE (a product of the lipoxygenase enzyme system) on basal and stimulated renin secretion from superficial cortical slices in the rat. First, rat cortex was shown to produce 12-HETE; chiral-phase high-performance liquid chromatography revealed that cortex produced 81% (S)-12-HETE and 19% (R)-12-HETE. (R)-12-HETE reduced basal renin release by 28 +/- 4% to 49 +/- 5% at concentrations of 10(-9) to 10(-7) M (P < 0.05 to 0.01). (S)-12-HETE did not significantly affect renin release. (R)-12-HETE also blunted isoproterenol-stimulated renin secretion (P < 0.05) at a concentration of 10(-6) M. 20-HETE, another cytochrome P-450 product, did not exert a significant effect on renin release. In summary, both (R)-12-HETE and (S)-12-HETE are synthesized by renal cortical tissue. Only (R)-12-HETE directly inhibits in vitro renin release. These findings suggest that the renal cytochrome P-450 enzyme system is capable of directly influencing local renin secretion.

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