Oxygen-derived radicals stimulate renin release of isolated juxtaglomerular cells

In anesthetized cats head-up tilting for 30 min and infusion of furosemide at 0.75 mg/kg in 30 min significantly raised renin release from the innervated kidney (increments of 90.7 +/- 21.4 ng/min on tilting and 105.4 +/- 26.4 ng/min after furosemide); a small and inconstant increase from the contralateral denervated kidney (increments of 16.8 +/- 16.0 and 16.3 +/- 17.7 ng/min, respectively) was abolished by acute bilateral adrenalectomy. Larger doses of furosemide (6.0 mg/kg) could release renin from the denervated kidney also, but the response was still more marked on the innervated side especially in the early period of infusion (increments of 132.7 +/- 23.8 and 33.7 +/- 23.8 ng/min of innervated and denervated sides at 10 min). The response of the denervated kidney to 6.0 mg furosemide/kg was not affected by adrenalectomy. Stimulation of juxtaglomerular cells by tilting is entirely due to sympathoadrenergic activation; stimulation by furosemide is also entirely neural when the diuretic drug is given in moderate doses, but is partly independent of innervation when larger doses are administered.

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Prostaglandins and renin release in vitro

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1981.240.6.e609 ◽

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.

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Do osmotic forces play a role in renin secretion?

AJP Renal Physiology ◽

10.1152/ajprenal.1988.255.1.f1 ◽

1988 ◽

Vol 255 (1) ◽

pp. F1-F10 ◽

Cited By ~ 8

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.

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Osmotically sensitive renin release from permeabilized juxtaglomerular cells

AJP Renal Physiology ◽

10.1152/ajprenal.1993.265.1.f87 ◽

1993 ◽

Vol 265 (1) ◽

pp. F87-F95 ◽

Cited By ~ 3

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.

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Abstract 141: Enhanced Hydrogen Peroxide-Dependent Renin and Pro-Renin Release in Juxtaglomerular Cells from Diabetic Mice: Role of NOX1

Hypertension ◽

10.1161/hyp.74.suppl_1.141 ◽

2019 ◽

Vol 74 (Suppl_1) ◽

Cited By ~ 1

Author(s):

M. Cecilia Ortiz-Capisano ◽

Dipak Maskey ◽

Mariela Mendez

Keyword(s):

Hydrogen Peroxide ◽

Renin Release ◽

Juxtaglomerular Cells ◽

Diabetic Mice

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Renin release: role of SNAREs

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00175.2014 ◽

2014 ◽

Vol 307 (5) ◽

pp. R484-R486 ◽

Cited By ~ 5

Author(s):

Mariela Mendez

Keyword(s):

Molecular Mechanism ◽

Current Knowledge ◽

Renin Release ◽

Juxtaglomerular Cells ◽

Attachment Protein ◽

Granule Exocytosis ◽

Protein Receptor ◽

Sensitive Factor ◽

Factor Attachment Protein Receptor

Little is known about the molecular mechanism mediating renin granule exocytosis and the identity of proteins involved. We previously showed that soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNAREs), a family of proteins required for exocytosis, mediate the stimulated release of renin from juxtaglomerular cells. This minireview focuses on the current knowledge of the proteins that facilitate renin-granule exocytosis. We discuss the identity of potential candidates that mediate the signaling and final steps of exocytosis of the renin granule.

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Calcium in the control of renin release

AJP Renal Physiology ◽

10.1152/ajprenal.1978.235.1.f22 ◽

1978 ◽

Vol 235 (1) ◽

pp. F22-F25 ◽

Cited By ~ 2

Author(s):

C. S. Park ◽

R. L. Malvin

Keyword(s):

Incubation Medium ◽

Inhibitory Action ◽

Inhibitory Effect ◽

Significant Inhibition ◽

Renin Release ◽

Juxtaglomerular Cells ◽

High K ◽

Intracellular Ca ◽

K Concentration ◽

Cortical Slices

The effect of Ca concentrations in the incubation medium and of estimated intracellular Ca concentrations on renin release was examined with use of pig renal cortical slices. In addition, the Ca requirement for the epinephrine stimulatory effect and for the ouabain inhibitory action on renin release was also tested. In mediums containing 5.9 mM K, variations in Ca concentration had no effect on renin release. In contrast, when the K concentration was 59 mM, a significant inhibition of renin release was attained with all concentrations of calcium. The inhibition of renin release in high K mediums by Ca was attributed to an increase in the intracellular Ca concentration. In addition, both the stimulatory effect of epinephrine and the inhibitory effect of ouabain on renin release required Ca in the medium. These results support the hypothesis that the control of renin secretion is mediated, in part, by changes in the intracellular concentration of Ca, most likely in the juxtaglomerular cells.

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