Correlation between secretagogue-induced Ca2+ influx, intracellular Ca2+ levels and secretion of catecholamines in cultured adrenal chromaffin cells

doi:10.1016/0197-0186(96)83614-X

Neurochemistry International

Volume 28, Issue 3, March 1996, Pages 325-334

https://doi.org/10.1016/0197-0186(96)83614-X Get rights and content

Abstract

Catecholamine secretion induced by various secretagogues in cultured bovine chromaffin cells has been correllated with Ca²⁺ influx and intracellular Ca²⁺ concentrations. Nicotine and high K⁺ caused prompt secretion of catecholamines from cells. Coincidently, both secretagogues evoked ⁴⁵[Ca²⁺] influx with a parallel increase in free intracellular Ca²⁺ concentration, as determined by Quin 2 fluorescence. However, the rate of return of Ca²⁺ level to baseline after nicotine stimulation was more rapid than after K⁺ stimulation. In comparison, stimulation with veratridine produced a slow and prolonged Ca²⁺ influx accompanied by lower levels of intracellular Ca²⁺ than those observed after nicotine or K⁺ stimulation. Yet, during 15 min of stimulation, veratridine induced a substantial catecholamine release, which was larger than that obtained after nicotine or K⁺ stimulations. The Ca²⁺ ionophore A23187 (1 μM) induced a pronounced increase in intracellular Ca²⁺ levels, but did not evoke any significant catecholamine release. Finally, addition of the Ca²⁺ channel blocker verapamil following stimulation, at a time when intracellular Ca²⁺ concentration was at its peak level, did not affect the rate of decline in intracellular free Ca²⁺ concentration but promptly blocked Ca²⁺ uptake and catecholamine secretion. These findings suggest that the rate of Ca²⁺ influx, rather than the absolute level of intracellular Ca²⁺ concentration, determines the rate and extent of catecholamine release.

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The calcium ionophore A23187 has been shown to affect the permeability of the cell membrane to Ca2+ and is used extensively to study the role of Ca2+ in cell regulation [31]. A23187 can induce extracellular Ca2+ influx and increase the intracellular Ca2+ concentration [32]. We added A23187 to the culture medium at different concentration for 1 h.
In S-RNase-based self-incompatibility, S-RNase was previously thought to function as a selective RNase that inhibits pollen whose S-haplotype matches that in the pistil. In this study, we showed that S-RNase has a distinct effect on the regulation of Ca²⁺-permeable channel activity in the apical pollen tube in Pyrus pyrifolia. While non-self S-RNase has no effect, self S-RNase decreases the activity of Ca²⁺ channels and disrupts the Ca²⁺ gradient at the tip of the growing pollen tube during the gametophytic self-incompatibility (GSI) response. Extracellular Ca²⁺ influx was suppressed 5 min after self S-RNase treatment, and self-pollen tube growth was reduced at 50 min after self S-RNase treatment. In the self-incompatible response, the expression of Ca²⁺-related genes was inhibited before RNA degradation. Therefore, self S-RNase suppresses Ca²⁺ influx prior to arresting pollen tube growth via RNA degradation.
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We have reported that natriuretic effects of K⁺ are involved in enhancement of renal kallikrein–kinin system. The study was aimed to examine 1) comparison of augmentative effects of K⁺ on urinary KK excretion with non-specific washout effects by trichlormethiazide (thiazide), polyethyleneglycol 200 (PEG) and rapid physiological saline infusion, 2) contribution of Ca²⁺ on the K⁺-induced increase in renal kallikrein secretion. Renal kallikrein activities were measured as fluorescence activities of methylcoumarinylamide-labeled synthetic substrate of tissue kallikrein (TK). Increases in urinary TK excretion were simultaneously observed with diuresis caused by thiazide, PEG, and rapid saline infusion. K⁺ infusion increased urinary TK excretion with a diuretic response same as the control. K⁺, but not thiazide, showed an early increase in renal TK secretion dose dependently in the kidney slices. Increases in renal TK secretion persisted during treatment with K⁺. Neither voltage-dependent Ca²⁺-channel blockers such as verapamil and nifedipine nor simultaneous treatment of EDTA affected on the K⁺-induced increase in renal TK secretion. While, EDTA decreased the K⁺-induced increases in renal TK secretion with time. Caffeine also had an early effect on the increase in renal TK secretion. K⁺-induced increases in renal TK secretion was demonstrated even after treatment with ryanodine or depletion of caffeine-sensitive intracellular Ca²⁺ by thapsigargin. It was indicated that the increase in renal TK secretion by K⁺ depends on the intracellular Ca²⁺ and the caffeine-sensitive release of intracellular Ca²⁺ may not be involved in this response. Mechanisms for the K⁺-induced increase in renal TK secretion needs to be further elucidated.
N-(4-Trifluoromethylphenyl)amide group of the synthetic histamine receptor agonist inhibits nicotinic acetylcholine receptor-mediated catecholamine secretion
2006, Biochemical Pharmacology
Citation Excerpt :
We also found that the increase in calcium induced by 60 mM K+ was not inhibited by pretreatment with 10 μM histamine-trifluoromethyltoluide, suggesting that voltage-dependent calcium channels are not affected by histamine-trifluoromethyltoluide (Fig. 8). In bovine adrenal chromaffin cells, veratridine-induced activation of sodium channels is known to cause membrane depolarization [24,25], thereby leading to a slow and weak increase in calcium through voltage-sensitive calcium channels [26]. We found that histamine-trifluoromethyltoluide had no effect on this veratridine-induced calcium increase (Fig. 8).
The therapeutic targeting of nicotinic receptors requires the identification of drugs that selectively activate or inhibit a limited range of nicotine acetylcholine receptors (nAChRs). In this study, we identified N-(4-trifluoromethylphenyl)amide group of the synthetic histamine receptor ligands, histamine-trifluoromethyltoluide, that act as potent inhibitors of nAChRs in bovine adrenal chromaffin cells. Catecholamine secretion induced by the nAChRs agonist, 1,1-dimethyl-4-phenylpiperazinium iodide (DMPP), was significantly inhibited by histamine-trifluoromethyltoluide. Real time carbon-fiber amperometry confirmed the ability of histamine-trifluoromethyltoluide to inhibit DMPP-induced exocytosis in single chromaffin cells. We also found that histamine-trifluoromethyltoluide inhibited DMPP-induced [Ca²⁺]_i and [Na⁺]_i increases, as well as DMPP-induced inward currents in the absence of extracellular calcium. Histamine-trifluoromethyltoluide had no effect on [³H]nicotine binding or on calcium increases induced by high K⁺, bradykinin, veratridine, histamine, and benzoylbenzoyl ATP. Among the synthetic histamine receptor ligands, clobenpropit exhibited similarity. In addition, 4′-nitroacetanilide also significantly attenuated nAChR-mediated catecholamine secretion. In conclusion, the N-(4-trifluoromethylphenyl)amide group of the histamine-trifluoromethyltoluide might be the critical moiety in the inhibition of nAChR-mediated CA secretion.
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Veratridine is a plant alkaloid that opens voltage-sensitive sodium channels by binding to the pharmacological site 2 on the sodium channels and slowing its inactivation [11]. In bovine adrenal chromaffin cells, veratridine-induced activation of sodium channels is known to cause membrane depolarization [12,13] thereby leading to slow and weak calcium increase through voltage-sensitive calcium channels [14]. The calcium increase by veratridine was not affected by borneol, either.
We previously reported that the aqueous extract from a medicinal plant Dryobalanops aromatica specifically inhibits the nicotinic acetylcholine receptor (nAChR) (Oh et al. Pharmacol Res 2000;42(6):559–64). Here, the effect of borneol, the main constituent of D. aromatica, on nAChR activity was investigated in bovine adrenal chromaffin cells. Borneol inhibited a nAChR agonist 1,1-dimethyl-4-phenylpiperazinium iodide (DMPP)-induced calcium increase with a half maximal inhibitory concentration (ic₅₀) of 56±9 μM. In contrast, borneol did not affect the calcium increases induced by high K⁺, veratridine, and bradykinin. The sodium increase induced by DMPP was also inhibited by borneol with similar potency (49±12 μM), suggesting that the activity of nAChRs is inhibited by borneol. Borneol inhibited DMPP-induced secretion of [ $^{3} H$ ]norepinephrine with an ic₅₀ of 70±12 μM. Carbon-fiber amperometry also confirmed the inhibition of DMPP-induced exocytosis by borneol in single chromaffin cells. [ $^{3} H$ ]nicotine binding, however, was not affected by borneol. The inhibitory effect by borneol is more potent than the effect by lidocaine, a commonly used local anesthetic. The data suggest that borneol specifically inhibits the nAChR-mediated effects in a noncompetitive way.
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Correlation between secretagogue-induced Ca2+ influx, intracellular Ca2+ levels and secretion of catecholamines in cultured adrenal chromaffin cells

Abstract

TINS

Pharmac. Ther.

J. Biol. Chem.

Biochim. Biophys. Acta

Neurochem. Int.

Cell Calcium

Biochem. Biophys. Res. Chem.

Neuron

FEBS Lett.

Neuron

Biochim. Biophys. Acta

Progr. Brain Res.

Vitamins Hormones

Calcium requirements for secretion in bovine chromaffin cells

J. Physiol. (Lond.)

Syntaxin: a synaptic protein implicated in docking of synaptic vesicles at presynaptic active zones

Science

Kinetic analysis of secretion from permeabilized adrenal chromaffin cells reveals distinct components

J. Biol. Chem.

Calcium, the cytoskeleton and calpactin (anexin II) in exocytotic secretion from adrenal chromaffin and mammary epithelial cells

Biochem. Soc. Trans.

Stimulus-secretion coupling in excitable cells: a central role for calcium

J. Exp. Biol.

Correlation between secretagogue-induced Ca²⁺ influx, intracellular Ca²⁺ levels and secretion of catecholamines in cultured adrenal chromaffin cells