Sensitive osmometer function of juxtaglomerular cells in vitro.

Frederiksen, O.; Leyssac, P. P.; Skinner, Sandford L.

doi:10.1113/jphysiol.1975.sp011164

Cited by 48 publications

(30 citation statements)

References 15 publications

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“…6). Although surprising at first view, the observed stimulation of renin secretion by high [K+]o is in accordance with the findings of Beierwaltes et al (1981) and Frederiksen et al (1975), obtained with similar preparations of rat JG cells. It should be noted in this context that high extracellular potassium also stimulates renin secretion in the isolated perfused rat kidney (Fray 1980) and hog kidney slices if extracellular calcium is low, and inhibits it at normal or.…”

Section: Resultssupporting

confidence: 91%

Lack of direct evidence for a functional role of voltage-operated calcium channels in juxtaglomerular cells

Kurtz

Skøtt²,

Chegini

et al. 1990

Pfl�gers Arch

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Abstract. In this study we have examined the role of voltagegated calcium channels in the regulation of calcium in juxtaglomerular cells. Using a combination of patch-clamp and single-cell calcium measurement we obtained evidence neither for voltage-operated calcium currents nor for changes of the intracellular calcium concentration upon acute depolarizations of the cell membrane. Increases of the extracellular concentration of potassium to 80 mmol/1 depolarized the juxtaglomerular cells close to the potassium equilibrium potential, but did not alter the intracellular calcium concentration neither in patch-clamped nor in intact Furaester-loaded cells. Moreover, basal renin secretion from a preparation enriched in mouse juxtaglomerular cells and from rat glomeruli with attached juxtaglomerular cells was not inliibited when extracellular potassium was isoosmotically increased to 56 mmol/1. In mouse kidney slices, however, depolarizing potassium concentrations caused a delayed inhibition at 56 mmol/1 and a delayed stimulation of renin secretion at 110 mmol/1. Taken together, our study does not provide direct evidence for a role of voltage-activated calcium channels in the regulation of calcium and renin secretion in renal juxtaglomerular cells.

show abstract

Section: Resultssupporting

confidence: 91%

Lack of direct evidence for a functional role of voltage-operated calcium channels in juxtaglomerular cells

Kurtz

Skøtt²,

Chegini

et al. 1990

Pfl�gers Arch

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“…The lack of change in renin release in response to the addition of 0-5 % DMSO is in accordance with the prediction that volume changes should be minimal or absent due to the high permeability of cell membranes to DMSO. The reduced or abolished response in renin release (first challenge) to lowering superfusate osmolality by reducing the sucrose 152 L. BA UMBACH COLOHICINE AND CYTOCHALASIN IN RENIN RELEASE 153 concentration or the sodium chloride concentration is hardly an effect of the increased initial osmolality since previous studies on isolated glomeruli have shown that the response to a hypotonic challenge was independent of the initial total osmolality in the range 285-355 m-osmole/kg (Frederiksen et al 1975). A decreased permeability to renin is also unlikely, since DMSO caused no change in basal renin release.…”

Section: Discussionmentioning

confidence: 99%

“…Based on earlier observations (Frederiksen et al 1975;Baumbach, Leyssac & Skinner, 1976) it has been proposed that the renin release process under study is somehow coupled to the JG-cell volume and its active regulation. The effects of colchicine and the vinca alkaloids on renin release are difficult to interpret in this context.…”

Section: Discussionmentioning

confidence: 99%

Renin release from isolated rat glomeruli: effects of colchicine, vinca alkaloids, dimethylsulphoxide, and cytochalasins.

Baumbach¹

1980

The Journal of Physiology

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SUMMARY1. Preparations of isolated glomeruli were superfused and the effects of colchicine, the vinca alkaloids, and the cytochalasins A, B, D, and E investigated on basal renin release and the response of the glomeruli to osmotic stress.2. Colchicine (10-3 M) had no effect, whereas vinblastine and vincristine (10-5 M) caused a progressive increase in basal renin release from isolated glomeruli.3. After 60 min exposure to either colchicine or the vinca alkaloids, the first renin release response to a hypoosmotic challenge (reduction in sucrose or sodium chloride concentration) was depressed while that of the second (after 120 min exposure) was enhanced. 6. The normal response to the first 30 m-osmole/kg reduction in NaCl concentration (and medium osmolality) was abolished by 0-5 % DMSO. Rather, a depressed release compared to unstimulated control experiments was observed. The response to the second stimulus in the presence of DMSO was about half that of control experiments. 7. Following the first hypoosmotic stimulus (by lowering the concentrations of sucrose or NaCl) the cytochalasins A, B, D and E (5 jug/ml.) caused an increased release of renin which persisted throughout the length of the experiment. The cytochalasins used were equally potent in this respect.8. The results are in agreement with previous findings, suggesting that renin release from the juxtaglomerular cells adhering to isolated glomeruli is mediated through a mechanism different from exocytosis.

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“…Moreover, changes in renin secretion occurs only with a short delay after osmolarity changes. It has been demonstrated that the nature of osmotically active particles is important for their effect on renin secretion, the effect on exocytosis is directly related to the reflection coefficient of the particle (Frederiksen et al 1975). From this observation juxtaglomerular cells are assumed to behave as sensitive osmometers.…”

Section: Osmotic Forcesmentioning

confidence: 99%

Cellular control of renin secretion

Kurtz

Wagner

Reviews of Physiology, Biochemistry and Pharmacology

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Sensitive osmometer function of juxtaglomerular cells in vitro.

Cited by 48 publications

References 15 publications

Lack of direct evidence for a functional role of voltage-operated calcium channels in juxtaglomerular cells

Lack of direct evidence for a functional role of voltage-operated calcium channels in juxtaglomerular cells

Renin release from isolated rat glomeruli: effects of colchicine, vinca alkaloids, dimethylsulphoxide, and cytochalasins.

Cellular control of renin secretion

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