Calcium and the Control of Renin Secretion*

Fray, J. C. S.; Park, C. S.; Valentine, Andrea

doi:10.1210/edrv-8-1-53

Cited by 89 publications

(35 citation statements)

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“…5 18 and produces results similar to other techniques that lower [Ca ϩ2 ] i . We find similar results in the present study, and, furthermore, we show that both cAMP generation and renin release induced by lowering [Ca ϩ2 ] i can be blocked with a selective AC-V antagonist.…”

Section: Discussionsupporting

confidence: 65%

“…2 However, unlike most secretory cell types, the renin release from the JG cell has a paradoxical interaction with intracellular calcium in that renin secretion is inhibited by increased intracellular calcium ([Ca ϩ2 ] i ) and conversely stimulated by decreased [Ca ϩ2 ] i . [3][4][5] The question of how [Ca ϩ2 ] i and adenylyl cyclase might act or interact to regulate renin has been a longstanding subject of debate and investigation. 1,5 Recently, using a preparation of primary cultures of isolated mouse JG cells that seem to completely maintain their phenotype and release renin, 6 we found that a calcium-inhibitable form of adenylyl cyclase existed within the JG cell, suggesting that changes in [Ca ϩ2 ] i regulate adenylyl cyclase activity, and this could account for this paradoxical relationship between [Ca ϩ2 ] i and renin.…”

mentioning

confidence: 99%

“…[3][4][5] The question of how [Ca ϩ2 ] i and adenylyl cyclase might act or interact to regulate renin has been a longstanding subject of debate and investigation. 1,5 Recently, using a preparation of primary cultures of isolated mouse JG cells that seem to completely maintain their phenotype and release renin, 6 we found that a calcium-inhibitable form of adenylyl cyclase existed within the JG cell, suggesting that changes in [Ca ϩ2 ] i regulate adenylyl cyclase activity, and this could account for this paradoxical relationship between [Ca ϩ2 ] i and renin. We found that decreased [Ca ϩ2 ] i leads to an increase in cAMP and, subsequently, renin release from isolated JG cells.…”

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confidence: 99%

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Adenylyl Cyclase Isoform V Mediates Renin Release From Juxtaglomerular Cells

et al. 2007

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Abstract-We have shown previously that decreasing intracellular calcium in the juxtaglomerular cells increases both cAMP formation and renin release. We hypothesized that this is because of an interaction between intracellular calcium and the calcium-inhibitable isoform of adenylyl cyclase, type-V. We used primary cultures of juxtaglomerular cells isolated from C-57/B6 mice at 70% to 80% confluence. Western blots were performed on isolated juxtaglomerular cells using antibodies against either of the 2 calcium inhibitable isoforms of adenylyl cyclase, types-V and -VI. Only the antibody against adenylyl cyclase-V gave us a strong band at 120 kDa as expected. There are 9 isoforms of adenylyl cyclase. They all share a similar structure that includes an intracellular N terminus followed by 2 membrane-spanning domains alternating with 2 catalytic cytoplasmic loops. 7 There are 2 adenylyl cyclase isoforms, type-V (AC-V) and type-VI (AC-VI), which are both inhibited by micromolar concentrations of [Ca ϩ2 ] i . 8 Both isoforms are found in lipid rafts in either the cell or intracellular membrane regions. 9 In addition, AC-V and AC-VI share a high amino acid sequence identity, particularly in the regions that form the enzymes catalytic unit. 10 However, the N termini of the 2 isoforms are quite divergent. 7 It has been reported that, in nonexcitable cells, AC-VI colocalizes with the calcium entry channels in the cell membrane. 11 Thus, whereas the 2 enzymes share many properties, they may also have different interactions within the cell and have different compartmentalization (such as in the surface or on intracellular membranes).Previously, 6 using an antibody that does not discriminate between the 2 isoforms, we found that either 1 or both of these calcium-inhibitable adenylyl cyclases existed within the JG cell, and their presence could explain the paradoxical effect of how decreasing [Ca ϩ2 ] i could result in a cAMPmediated stimulation of renin secretion. Although we observed a provocative colocalization of our antibody with renin on what appeared to be granule-like foci within the cytoplasm, 6 we were unable to distinguish between the 2 isoforms to answer the critical question of which calciuminhibitable isoform of adenylyl cyclase is in the JG cell and

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Section: Discussionsupporting

confidence: 65%

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confidence: 99%

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confidence: 99%

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Adenylyl Cyclase Isoform V Mediates Renin Release From Juxtaglomerular Cells

et al. 2007

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“…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. high calcium concentrations (Churchill 1980(Churchill , 1987Matsumura 1984;Park et al 1981;Fray et al 1987, Fray 1980. Our finding that extracellular potassium at 56 mmol!…”

Section: Resultsmentioning

confidence: 60%

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.

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“…Such cells include osteoclasts (9,10), parathyroid chief cells (7,11), thyroid C cells ( 12,13), juxtaglomerular cells ( 14), enterocytes ( 15), and keratinocytes ( 16). Cationinduced activation of a given CaR results in the generation of intracellular signals that in turn modify cell function.…”

Section: Introductionmentioning

confidence: 99%

A ryanodine receptor-like molecule expressed in the osteoclast plasma membrane functions in extracellular Ca2+ sensing.

Zaidi

Shankar²,

Tunwell³

et al. 1995

J. Clin. Invest.

115

108

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Ryanodine receptors (RyRs) reside in microsomal membranes where they gate Ca2" release in response to changes in the cytosolic Ca2" concentration. In the osteoclast, a divalent cation sensor, the Ca2" receptor (CaR) Ca2" elevations induced by Ni2". In contrast, the responses to Ni2" were strongly potentiated by an antiserum Ab"2 raised to an epitope located within the channel-forming domain of the type II RyR. The antiserum also stained the surface of intact, unfixed, trypan blue-negative osteoclasts. Serial confocal sections and immunogold scanning electron microscopy confirmed a plasma membrane localization of this staining. Antiserum AbM directed to a putatively intracellular RyR epitope expectedly did not stain live osteoclasts nor did it potentiate CaR activation. It did, however, stain fixed, permeabilized cells in a distinctive cytoplasmic pattern. We conclude that an RyR-like molecule resides within the osteoclast plasma membrane and plays an important role in extracellular Ca2" sensing. (J. Clin. Invest. 1995.

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Calcium and the Control of Renin Secretion*

Cited by 89 publications

References 0 publications

Adenylyl Cyclase Isoform V Mediates Renin Release From Juxtaglomerular Cells

Adenylyl Cyclase Isoform V Mediates Renin Release From Juxtaglomerular Cells

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

A ryanodine receptor-like molecule expressed in the osteoclast plasma membrane functions in extracellular Ca2+ sensing.

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