Plasmalemmal sodium-calcium exchanger shapes the calcium and exocytotic signals of chromaffin cells at physiological temperature

2013 ◽  
Vol 305 (2) ◽  
pp. C160-C172 ◽  
Author(s):  
Juan-Fernando Padín ◽  
José-Carlos Fernández-Morales ◽  
Román Olivares ◽  
Stefan Vestring ◽  
Juan-Alberto Arranz-Tagarro ◽  
...  
Keyword(s):  
Chromaffin Cells ◽  
Catecholamine Release ◽  
Sodium Calcium Exchanger ◽  
Physiological Temperature ◽  
Slowing Down ◽  
Sodium Calcium ◽  
High K ◽  
Highly Sensitive ◽  
Bovine Chromaffin Cells ◽  
Kinetics Of

The activity of the plasmalemmal Na+/Ca2+ exchanger (NCX) is highly sensitive to temperature. We took advantage of this fact to explore here the effects of the NCX blocker KB-R7943 (KBR) at 22 and 37°C on the kinetics of Ca2+ currents ( ICa), cytosolic Ca2+ ([Ca2+]c) transients, and catecholamine release from bovine chromaffin cells (BCCs) stimulated with high K+, caffeine, or histamine. At 22°C, the effects of KBR on those parameters were meager or nil. However, at 37°C whereby the NCX is moving Ca2+ at a rate fivefold higher than at 22°C, various of the effects of KBR were pronounced, namely: 1) no effects on ICa; 2) reduction of the [Ca2+]c transient amplitude and slowing down of its rate of clearance; 3) blockade of the K+-elicited quantal release of catecholamine; 4) blockade of burst catecholamine release elicited by K+; 5) no effect on catecholamine release elicited by short K+ pulses (1–2 s) and blockade of the responses produced by longer K+ pulses (3–5 s); and 6) potentiation of secretion elicited by histamine or caffeine. Furthermore, the more selective NCX blocker SEA0400 also potentiated the secretory responses to caffeine. The results suggest that at physiological temperature the NCX substantially contributes to shaping the kinetics of [Ca2+]c transients and the exocytotic responses elicited by Ca2+ entry through Ca2+ channels as well as by Ca2+ release from the endoplasmic reticulum.

Faster kinetics of quantal catecholamine release in mouse chromaffin cells stimulated with acetylcholine, compared with other secretagogues

2016 ◽  
Vol 139 (5) ◽  
pp. 722-736 ◽  
Author(s):  
Enrique Calvo-Gallardo ◽  
Ángela López-Gil ◽  
Iago Méndez-López ◽  
Carmen Martínez-Ramírez ◽  
Juan Fernando Padín ◽  
...  
Keyword(s):  
Chromaffin Cells ◽  
Catecholamine Release ◽  
Kinetics Of

Different contributions of L- and Q-type Ca2+ channels to Ca2+ signals and secretion in chromaffin cell subtypes

1997 ◽  
Vol 272 (2) ◽  
pp. C476-C484 ◽  
Author(s):  
R. B. Lomax ◽  
P. Michelena ◽  
L. Nunez ◽  
J. Garcia-Sancho ◽  
A. G. Garcia ◽  
...  
Keyword(s):  
Chromaffin Cells ◽  
Chromaffin Cell ◽  
Channel Blocker ◽  
Cell Types ◽  
Bay K 8644 ◽  
High K ◽  
Voltage Dependent ◽  
Bovine Chromaffin Cells ◽  
P Type ◽  
Ca2 Channels

In this study, we investigated the contribution of different subtypes of voltage-dependent Ca2+ channels to changes in cytosolic free Ca2+ ([Ca2+]i) and secretion in noradrenergic and adrenergic bovine chromaffin cells. In single immunocytochemically identified chromaffin cells, [Ca2+]i increased transiently during high K+ depolarization. Furnidipine and BAY K 8644, L-type Ca2+ channel blocker and activator, respectively, affected the [Ca2+]i rise more in noradrenergic than in adrenergic cells. In contrast, the Q-type Ca2+ channel blocker omega-conotoxin MVIIC inhibited the [Ca2+]i rise more in adrenergic cells. omega-Agatoxin IVA (30 nM), which blocks P-type Ca2+ channels, had little effect on the [Ca2+]i signal. The N-type Ca2+ channel blocker omega-conotoxin GVIA similarly inhibited the [Ca2+]i rise in both cell types. The effects of furnidipine, BAY K 8644, and omega-conotoxin MVIIC on K+-evoked norepinephrine and epinephrine release paralleled those effects on [Ca2+]i signals. However, omega-conotoxin GVIA and 30 nM omega-agatoxin IVA did not affect the secretion of either amine. The data suggest that, in the bovine adrenal medulla, the release of epinephrine and norepinephrine are preferentially controlled by Q- and L-type Ca2+ channels, respectively. P- and N-type Ca2+ channels do not seem to control the secretion of either catecholamine.

Calcium export by sodium-calcium exchange in bovine chromaffin cells

Cell Calcium ◽  
1991 ◽  
Vol 12 (7) ◽  
pp. 493-504 ◽  
Author(s):  
D.A. Powis ◽  
K.J. O'Brien ◽  
H.R.K. Von Grafenstein
Keyword(s):  
Chromaffin Cells ◽  
Sodium Calcium ◽  
Bovine Chromaffin Cells ◽  
Calcium Exchange ◽  
Sodium Calcium Exchange

Pb2(+)-induced secretion from bovine chromaffin cells: fura-2 as a probe for Pb2+

1990 ◽  
Vol 259 (5) ◽  
pp. C762-C768 ◽  
Author(s):  
J. L. Tomsig ◽  
J. B. Suszkiw
Keyword(s):  
Dissociation Constant ◽  
Chromaffin Cells ◽  
Ionic Composition ◽  
Catecholamine Release ◽  
Apparent Dissociation Constant ◽  
Fura 2 ◽  
Bovine Chromaffin Cells ◽  
In Cells

The effect of Pb2+ on catecholamine release was studied in isolated intact and permeabilized bovine chromaffin cells. Fura-2 was used to monitor intracellular Pb2+. A characterization of Pb2(+)-fura-2 interactions in solutions simulating intracellular ionic composition showed that Pb2+ forms a 1:1 Pb2(+)-fura-2 complex (apparent dissociation constant = 4.2 x 10(-12) M, pH 7.05) whose fluorescence resembles that of the Ca2(+)-fura-2 complex. Spectra recorded from fura-2-loaded cells indicate entry of Pb2+ into the cells. Intracellular Pb2+ concentrations were proportional to extracellular Pb2+ concentrations and were found to be 10(-11)-10(-12) M in cells exposed to micromolar Pb2+ concentrations. Pb2+ elicited the release of tritiated norepinephrine from fura-2-loaded cells, indicating the extraordinary effectiveness of Pb2+ as a releasing agent. Permeabilization of cells with digitonin showed that Pb2+ is able, in the absence of Ca2+, to produce exocytotic release at concentrations of 3.2 x 10(-10) M or higher (3 orders of magnitude lower than Ca2+). These results support the notion that Pb2+ can act as a potent Ca2+ surrogate in triggering secretion.

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