Extracellular calcium exerts a dual effect on renin secretion from isolated mouse juxtaglomerular cells

Schricker, K. Th.; Bruna, Roberto Della; Kurtz, Armin

doi:10.1007/bf00374955

Cited by 12 publications

(3 citation statements)

References 33 publications

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“…Studies with permeabilized JG cells produced the interesting result that renin secretion in this preparation is actually stimulated by high calcium concentration what would fit with the ‘classic’ mode of action of calcium on exocytosis (Jensen & Skott 1994). A delayed stimulatory effect of high extracellular calcium concentrations on renin secretion has also been seen in primary cultures of JG cells (Schricker et al. 1993).…”

Section: The Effects Of Calcium On Renin Releasementioning

confidence: 87%

Cellular mechanism of renin release

Schweda

Kurtz

2004

Acta Physiologica Scandinavica

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In this review we aim to give a comprehensive overview over the current knowledge of the cellular control of renin release. We hereby focus on the inhibitory effects of calcium on the exocytosis of renin. After a short introduction into general aspects of the regulation of renin release, including a brief summary on the role of the second messengers cAMP and cGMP, we will discuss parts of the literature on the effects of calcium on the renin system together with recent studies from our laboratory, investigating putative calcium influx and extrusion pathways of juxtaglomerular cells. Finally, as the precise mechanisms by which calcium inhibits the exocytosis of renin are far from being understood, we will present some hypotheses on the intracellular events being involved in the suppression of renin release by calcium.

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Section: The Effects Of Calcium On Renin Releasementioning

confidence: 87%

Cellular mechanism of renin release

Schweda

Kurtz

2004

Acta Physiologica Scandinavica

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“…Endothelins induced calcium oscillations in juxtaglomerular cells that were dependent on extracellular calcium and that were associated with prominent calcium-activated chloride currents (manuscript in preparation). Calcium mobilization is thought to be essentially involved in the regulation of renin secretion from juxtaglomerular cells [14]. Endothelin's effects on stimulated renin secretion may be one factor responsible for inhibition of renin release in coculture with endothelial cells [1,8,9].…”

Section: Role Of Endothelial Mediators For Renin Release From Isolatementioning

confidence: 99%

Endothelium-mediated regulation of renin secretion

Krämer

Ritthaler

Ackermann

et al. 1994

Kidney International

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The aim of the present study was to investigate the endothelial influence on renin secretion of isolated juxtaglomerular cells. Specifically the role of nitric oxide (NO) and of endothelin was studied. Coculture of primary cultures of juxtaglomerular cells with aortic and microvascular endothelial cells decreased renin secretion. Inhibition of NO formation by absence of l-arginine or presence of N omega-nitro-l-arginine caused a marked decrease in cGMP accumulation and a reduction in renin secretion in cocultures. Exogenous NO (NO liberators sodium nitroprusside/SIN 1) stimulated the 20-hour renin secretion from juxtaglomerular cells markedly, too. The effect of NO on renin secretion was biphasic: short-time inhibition and long-time stimulation of renin release. NO's stimulatory effect on renin secretion is dependent on extracellular calcium, but independent on cAMP or cGMP accumulation. Endothelin 1, 2, and 3 did not affect basal renin secretion, but inhibited cAMP stimulated renin release to a similar extent. Endothelin's action is not mediated via the subtype A endothelin receptor, but seems to involve calcium mobilization in juxtaglomerular cells that is dependent on extracellular calcium and associated with prominent calcium activated chloride channels. Taken together, coculture of juxtaglomerular cells with endothelial cells inhibits renin secretion despite the stimulatory effect of native NO released from endothelial cells. cAMP stimulated renin secretion is inhibited by all three endothelin isoforms thus contributing to the inhibition of renin secretion in coculture.

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“…In vivo, there seems thus to be a lag period before the renin secretion in the juxtaglomerular cells is stimulated by the reduced intracellular Ca" concen¬ tration, provoked by the high dietary calcium intake. In vitro, in primary cultures of mouse renal juxtaglomerular cells, an increase in extracellular calcium had a dual effect on renin secretion (Schricker et al 1993): an inhibitory one that lasted for at least 1 h and a powerful stimulatory one that occurred with a delay of approximately 1-3 h.…”

Section: ) Actionsmentioning

confidence: 98%

Effect of oral calcium supplementation on intracellular calcium and plasma renin in men

Lijnen

Petrov²

1995

Journal of Endocrinology

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A double-blind, placebo-controlled parallel study was conducted on the effect of a high daily oral calcium supplementation of 1 g elemental calcium, given twice daily for 16 weeks in normal male subjects, on plasma renin, aldosterone, kallikrein, cGMP, cAMP and calciotropic hormones, intracellular calcium concentrations and plasma total and ionized calcium. After a 1-month run-in period on a limited use of dairy products, the subjects (n = 32) were allocated to a placebo or a calcium group. Placebo or 1 g elemental calcium was administered twice daily in the morning and evening for 16 weeks. All subjects were investigated at baseline and after 1, 2, 4, 8 and 16 weeks of placebo or calcium administration. A decreased intraerythrocyte and intraplatelet Ca2+ concentration was observed in the calcium-treated subjects. Compared with the placebo group, an increase in the plasma renin activity (PRA) in the calcium group was observed after 4, 8 and 16 weeks of oral calcium administration. However, plasma aldosterone and urinary excretion of aldosterone, kallikrein, cGMP and cAMP were not changed during calcium administration. Oral calcium supplementation in these men was also accompanied by a reduction in the plasma concentration of intact parathyroid hormone and 1,25-dihydroxyvitamin D3, an increase in 24-h urinary calcium excretion but no change in the plasma total Ca2+ concentration, serum ionized Ca2+ level and plasma phosphate or 25-hydroxyvitamin D3. Lacidipine tended to increase PRA in the placebo-treated subjects and to decrease it in the calcium-treated subjects: this difference in lacidipine effect between the placebo and calcium group was significant (P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

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Extracellular calcium exerts a dual effect on renin secretion from isolated mouse juxtaglomerular cells

Cited by 12 publications

References 33 publications

Cellular mechanism of renin release

Cellular mechanism of renin release

Endothelium-mediated regulation of renin secretion

Effect of oral calcium supplementation on intracellular calcium and plasma renin in men

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