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

Abstract

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.

Molecular and Functional Identification of Cyclic AMP-Sensitive BK Ca Potassium Channels (ZERO Variant) and L-Type Voltage-Dependent Calcium Channels in Single Rat Juxtaglomerular Cells

“…23 This may explain why it was not possible to observe an increase in Ca 2ϩ i using a depolarizing voltage step protocol. 4,5 When depolarizing a similar preparation with K ϩ , Russ and coworkers 23 reported a small dose-dependent increase in Ca 2ϩ i that was abolished by a dihydropyridine Ca 2ϩ antagonist. In many smooth muscle cells, a global increase in intracellular calcium concentration after calcium influx depends on calcium-induced calciumrelease from intracellular stores via ryanodine or IP 3 receptors.…”

Physiology of Kidney Renin

“…In addition, an increase in the extracellular K ϩ concentration or an inhibition of K ϩ channels not only depolarizes JG cells, but also suppresses renin release (158,269,480,487). On the other hand, the membrane hyperpolarization induced by K ϩ channel activation or Cl Ϫ channel inhibition is accompanied by a stimulated renin secretion (227,239,396,403,615).…”

ATP-sensitive K+ channels in the kidney

“…2); conversely, blockade of the KAy P channel could increase [Ca2+]i , thus decreasing the rate of renin secretion. Obviously, this working model requires testing; the fact that juxtaglomerular cells lack the voltage-dependent Ca 2+ channel characteristic of smooth muscle cells (Kurtz and Penner 1989;Kurtz et al 1990;Scholz and Kurtz 1995) demonstrates that the two cell types differ substantially in their electrophysiological properties.…”