Sodium-dependent and sodium-independent nicotine-evoked catecholamine release from cat adrenals

Abajo, F.J.; Castro, María Antonia S.; Lopo, C.R.; Garijo, B; Sánchez‐García, P.; Garcı́a, Antonio G.

doi:10.1016/0304-3940(89)90448-5

Cited by 5 publications

(4 citation statements)

References 19 publications

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“…inhibition of secretion by specific Ca channel antagonists) it seemed to us that both nicotinic and high-K-mediated catecholamine release were triggered by the same type of Ca channels (Cefia et al, 1983). This is supported by the observation that (+)-isradipine (a 1,4-dihydropyridine derivative) blocks the nicotinic response only in the presence of Na (Cirdenas et al, 1988;Abajo et al, 1989). Therefore, it is likely that Na entering through the acetylcholine receptor ionophore (Amy & Kirshner, 1982;Wada et al, 1985) causes cell depolarization and opening of Ca channels.…”

Section: Introductionmentioning

confidence: 94%

Separation of two pathways for calcium entry into chromaffin cells

Gandı́a

Casado

López

et al. 1991

British J Pharmacology

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1 The effects of various drugs on 45Ca + 40Ca uptake into cultured bovine adrenal chromaffin cells evoked by 1,1-dimethyl-4-phenylpiperazinium (DMPP) or high K, were studied. In the presence of 1 mm external 40Ca, with 45Ca as a radiotracer, unstimulated cells took up an average of 0.13 fmol/cell 40Ca and 772 c.p.m./106 cells of 45Ca (n = 76). Upon stimulation with DMPP (100,pM for 60 s) or K (59 mm for 60 s), Ca uptake increased to 0.92 and 1 fmol/cell, respectively.2 Flunarizine behaved as a potent blocker of both DMPP-and K-evoked Ca uptake (IC50 of 1.76 and 1.49,M, respectively for DMPP and K). A similar picture emerged with Cd ions, though Cd exhibited an IC50 against K (1.86pM) slightly lower than the IC50 against DMPP (8.14pM).3 Clear cut differences were observed with amiloride, guanethidine, nimodipine and nisoldipine which behaved as selective blockers of DMPP-mediated Ca uptake responses: IC50 values to block DMPP effects were 290, 27, 1.1 and 1.63,UM respectively for amiloride, guanethidine, nimodipine and nisoldipine.Amiloride blocked K-evoked Ca uptake by only 35% and guanethidine did not affect it. Nisoldipine inhibited K-evoked Ca uptake only partially at low concentrations (about 30%); a second blocking component was observed at the highest concentration used (10pM). At 10pM, nimodipine blocked K-evoked Ca uptake by 50%. 4 Thus, it seems that the nicotinic receptor mediated Ca uptake pathway can be pharmacologically separated from the K-activated pathway. The results are compatible with the hypothesis that in cultured bovine adrenal chromaffin cells, stimulation of nicotinic receptors recruits a single type of Ca channel which is sensitive to flunarizine, Cd, amiloride, guanethidine, nimodipine and nisoldipine. The results also suggest that K depolarization might be recruiting in addition to this channel, another Ca channel which is highly sensitive to Cd and flunarizine, resistant to nisoldipine, nimodipine and amiloride, and insensitive to guanethidine.

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Section: Introductionmentioning

confidence: 94%

Separation of two pathways for calcium entry into chromaffin cells

Gandı́a

Casado

López

et al. 1991

British J Pharmacology

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“…Action potentials induce nerve terminal membrane depolarization after which the calcium ion enters from the extracellular space through the opening calcium channels (Illes, 1986). The requirement of calcium ions for a nicotine-induced NA release is generally accepted (Jayasundar & Vohra, 1977;Starke & Weitzell, 1978;Kirpekar et al, 1980;Abajo et al, 1989). However, the information about the characterization of calcium channels in nicotine-induced functional responses and NA release is not known with any degree of certainty.…”

Section: Introductionmentioning

confidence: 99%

“…As VOCCs on the nerve terminals were not activated, the vasoconstrictor responses to nicotine and ACh were not affected by w-CgTX. However, the requirement of calcium ions for the nicotine-induced NA release is generally accepted (Jayasundar & Vohra, 1977;Starke & Weitzell, 1978;Kirpekar et al, 1980;Abajo et al, 1989). Calcium ions might enter the nerve terminals through other kinds of calcium ion channels.…”

Section: Vascular Responses To Nicotine and Achmentioning

confidence: 99%

Differential effects of ω‐conotoxin GVIA and tetrodotoxin on vasoconstrictions evoked by electrical stimulation and nicotinic receptor stimulation in canine isolated, perfused splenic arteries

Ren¹,

Nakane²,

Chiba³

1994

British J Pharmacology

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1 The effects of w-conotoxin GVIA (Qo-CgTX) and tetrodotoxin (TTX) on vasoconstrictions induced by acetylcholine (ACh) and nicotine were investigated and compared with those induced by periarterial electrical stimulation in the isolated and perfused canine splenic arteries. 5 Vascular responses to ACh were completely inhibited by 1 pmol hexamethonium. In the preparations treated with 100 nmol nicotine, ACh did not produce any vasoconstriction. However, the NA-induced vasoconstriction was affected by neither hexamethonium nor nicotine treatment. 6 Atropine (1 ftM) significantly inhibited but did not abolish the vasoconstrictor responses to ACh. The vascular responses to nicotine and NA were also significantly inhibited by atropine treatment. 7 These results indicate that (1) ACh constricts the splenic artery through the activation of presynaptic nicotinic receptors present on the sympathetic nerves; (2) differential effects of TTX and w-CgTX on the vascular responses to ACh and nicotine, and to electrical stimulation suggest that the receptor-operated ion channels are mainly responsible for NA release induced by nicotinic receptor stimulation, but N-type VOCCs are responsible for that by electrical stimulation; (3) atropine may have an inhibitory action on nicotine-related responses, in addition to its inhibitory action on NA.

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“…Cardiac sodium and calcium channels: The binding of nicotine to the extracellular binding site of the nicotinic acetylcholine receptor leads to a conformational change of the central pore, which results in the influx of sodium and calcium ions [73,74]. In addition to the increase in intracellular calcium concentration facilitated by sodium influx through the nicotine receptor [73], nicotine also evokes calcium influx by direct activation of voltagedependent calcium channels [75][76][77]. More specifically, the L-type Ca2+ channels-Cav 1.2 channel, in particular-have been implicated in nicotine addiction, and are controlled by the SNS and stimulated by nicotine [78,79].…”

Section: Cardiac Autonomic Nervous Systemmentioning

confidence: 99%

The effects of nicotine and cigarette smoking on cardiac electrophysiology.

Irfan¹

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collaboration, and contribution to projects related to this dissertation. This work would not have been possible without the administrative and financial support of Marshall University's Departments of Cardiology and Clinical Translational Services. I am especially grateful to research coordinators, Melissa Marcum and Scott Wiley, for their perseverance and unwavering commitment to this research study. I am greatly indebted to, and honored by, the encouragement and guidance from Dr. Christian Mueller, who introduced me to cardiovascular research and helped take the first steps of my scientific pursuits. Lastly, I thank my dear family, especially my mother, father, brother, sister, and wife for their enduring love, support, and sacrifice.

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Sodium-dependent and sodium-independent nicotine-evoked catecholamine release from cat adrenals

Cited by 5 publications

References 19 publications

Separation of two pathways for calcium entry into chromaffin cells

Separation of two pathways for calcium entry into chromaffin cells

Differential effects of ω‐conotoxin GVIA and tetrodotoxin on vasoconstrictions evoked by electrical stimulation and nicotinic receptor stimulation in canine isolated, perfused splenic arteries

The effects of nicotine and cigarette smoking on cardiac electrophysiology.

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