Tetraethylammonium stimulates adrenomedullary secretion by causing fluctuations in a cytosolic free Ca concentration

Sorimachi, Masaru; Yamagami, Kazuhiko; Nishimura, Shigeto

doi:10.1016/0006-8993(90)90296-n

Cited by 17 publications

(7 citation statements)

References 13 publications

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“…After an initial secretary peak (around 2000 ng 30 s-1) the rate of catecholamine release declined to a plateau at around 700 ng 30 s-5. Stimulation by TEA of catecholamine release from perfused cat adrenals was previously reported by Kirpekar, Prat & Schiavone (1983); they attributed this effect to depolarization by TEA of chromaffin cells which, as demonstrated later on, caused marked fluctuations in cytosolic Ca2+ concentrations (Sorimachi, Yamagami & Nishimura, 1990). Effects of d-tubocurarine and apamin on cytosolic C(ia2 signals evoked by methacholine The hypothesis raised in this study implies that Ca2+-dependent K+ channels might shape the methacholine secretary profile.…”

Section: Effects Of Apamin On Methacholine-induced Secretionsupporting

confidence: 67%

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Ca(2+)‐activated K+ channels modulate muscarinic secretion in cat chromaffin cells.

Uceda

Artalejo

López

et al. 1992

The Journal of Physiology

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G. UCEDA AND OTHERS Depolarization is probably counteracted by activation of CaFt-dependent K+ channels. Therefore, inhibition of these channels enhances depolarization and firing of action potentials which activate voltage-dependent L-type Ca2+ channels to increase further the CaF+ signal and the secretary response. Thus Ca2+-dependent K+ channels, probably of the small-conductance type (SK), seem to be involved in the modulation of muscarinic-evoked catecholamine release responses in cat adrenal chromaffin cells.

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Section: Effects Of Apamin On Methacholine-induced Secretionsupporting

confidence: 67%

“…In contrast, TEA enhanced it markedly. This increase has been attributed to direct depolarizing effects of TEA in cat chromaffin cells (Sorimachi et al 1990) probably associated with direct nicotinic receptor stimulation. In fact, DTC blocked the TEA-evoked secretary response (not shown).…”

Section: Discussionmentioning

confidence: 99%

Ca(2+)‐activated K+ channels modulate muscarinic secretion in cat chromaffin cells.

Uceda

Artalejo

López

et al. 1992

The Journal of Physiology

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“…S4) is consistent with studies showing that BK channels of chromaffin cells modulate the release of catecholamines, which modulate via adrenergic receptors the release of aldosterone. The role of the BK-␣/␤1 in regulating catecholamine release may be similar to its role in other tissues, having an effect to hyperpolarize the membrane potential and mitigate the Camediated release of catecholamines (39,40). Catecholamineinduced elevations in glomerulosa cAMP levels stimulate Ca influx via L-type Ca channels (41,42), leading to increased aldo production and release.…”

Section: Discussionmentioning

confidence: 99%

Hypertension of Kcnmb1 ^−/− is linked to deficient K secretion and aldosteronism

Grimm

Irsik

Settles

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

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Mice lacking the ␤1-subunit (gene, Kcnmb1; protein, BK-␤1) of the large Ca-activated K channel (BK) are hypertensive. This phenotype is thought to result from diminished BK currents in vascular smooth muscle where BK-␤1 is an ancillary subunit. However, the ␤1-subunit is also expressed in the renal connecting tubule (CNT), a segment of the aldosterone-sensitive distal nephron, where it associates with BK and facilitates K secretion. Because of the correlation between certain forms of hypertension and renal defects, particularly in the distal nephron, it was determined whether the hypertension of Kcnmb1 ؊/؊ has a renal origin. We found that Kcnmb1 ؊/؊ are hypertensive, volume expanded, and have reduced urinary K and Na clearances. These conditions are exacerbated when the animals are fed a high K diet (5% K; HK). Supplementing HK-fed Kcnmb1 ؊/؊ with eplerenone (mineralocorticoid receptor antagonist) corrected the fluid imbalance and more than 70% of the hypertension. Finally, plasma [aldo] was elevated in Kcnmb1 ؊/؊ under basal conditions (control diet, 0.6% K) and increased significantly more than wild type when fed the HK diet. We conclude that the majority of the hypertension of Kcnmb1 ؊/؊ is due to aldosteronism, resulting from renal potassium retention and hyperkalemia.adrenal medulla ͉ BK ͉ eplerenone ͉ mineralcorticoid ͉ volume expansion

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“…In PC12 cells, Di Virgilio et al (1987) reported that elevation of [K + ] o to 50 m M was enough to alter significatnly the membrane potential, which consequently activated the voltage‐sensitive calcium channels and markedly enhanced the [Ca 2+ ] i in the presence of extracellular calcium. By blocking K + channels, TEA was found to increase indirectly the Ca 2+ influx via depolarizing the cell membrane and in turn to stimulate catecholamine secretion in bovine adrenal chromaffin cells, the nontumoral counterpart of PC12 cells (Sorimachi et al, 1990). Another K + channel blocker, BaCl 2 , was also found to cause membrane depolarization in several tissues and cells, including the rat brain synaptosomes (Sihra et al, 1993) and bovine adrenal chromaffin cells (von Rüden et al, 1993).…”

Section: Discussionmentioning

confidence: 99%

Modulation of Dopamine Transporter Activity by Nicotinic Acetylcholine Receptors and Membrane Depolarization in Rat Pheochromocytoma PC12 Cells

Huang¹,

Chen²,

Huang³

et al. 1999

Journal of Neurochemistry

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Abstract:To elucidate the regulation of the rat dopamine transporter (rDAT), we established several PC12 variants overexpressing the rDAT. Treating these cells with a nicotinic agonist (1,1-dimethyl-4-phenylpiperazinium iodide, 30 M) depolarized the plasma membrane potential from Ϫ31 Ϯ 2 to 43 Ϯ 5 mV and inhibited rDAT activity significantly in a calcium-and protein kinase C-independent manner. Membrane depolarization by a high external K ϩ concentration or two K ϩ channel blockers (tetraethylammonium hydroxide and BaCl 2 ) also resulted in a marked inhibition of rDAT activity. Such inhibition of dopamine uptake is due to a reduction in V max , with no marked effect on the K m for dopamine. The potency of cocaine in inhibiting dopamine uptake was not significantly altered, whereas that of amphetamine was slightly enhanced by membrane depolarization. Removing extracellular Ca 2ϩ or blocking the voltage-sensitive L-type calcium channels using nifedipine did not exert any significant effect on the inhibition of rDAT activity by depolarization. These data confirm that calcium influx on depolarization is not required for inhibition of the rDAT. Collectively, our data suggest that rDAT activity can be altered by a neurotransmitter that modulates the membrane potential, thus suggesting an exquisite mechanism for the fine-tuning of dopamine levels in the synapse. Key Words: Dopamine transporter-Nicotinic acetylcholine receptor-Depolarization-Protein kinase C-Calcium.

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Tetraethylammonium stimulates adrenomedullary secretion by causing fluctuations in a cytosolic free Ca concentration

Cited by 17 publications

References 13 publications

Ca(2+)‐activated K+ channels modulate muscarinic secretion in cat chromaffin cells.

Ca(2+)‐activated K+ channels modulate muscarinic secretion in cat chromaffin cells.

Hypertension of Kcnmb1 ^−/− is linked to deficient K secretion and aldosteronism

Modulation of Dopamine Transporter Activity by Nicotinic Acetylcholine Receptors and Membrane Depolarization in Rat Pheochromocytoma PC12 Cells

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Tetraethylammonium stimulates adrenomedullary secretion by causing fluctuations in a cytosolic free Ca concentration

Cited by 17 publications

References 13 publications

Ca(2+)‐activated K+ channels modulate muscarinic secretion in cat chromaffin cells.

Ca(2+)‐activated K+ channels modulate muscarinic secretion in cat chromaffin cells.

Hypertension of Kcnmb1 −/− is linked to deficient K secretion and aldosteronism

Modulation of Dopamine Transporter Activity by Nicotinic Acetylcholine Receptors and Membrane Depolarization in Rat Pheochromocytoma PC12 Cells

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Hypertension of Kcnmb1 ^−/− is linked to deficient K secretion and aldosteronism