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  • 1
    Electronic Resource
    Electronic Resource
    Protein Kinase C-Mediated Down-Regulation of Voltage-Dependent Sodium Channels in Adrenal Chromaffin Cells (1996)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 66 (1996), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Treatment of cultured bovine adrenal chromaffin cells with 12-O-tetradecanoylphorbol 13-acetate (TPA), an activator of protein kinase C (PKC), decreased [3H]saxitoxin ([3H]STX) binding in a concentration (IC50 = 19 nM)- and time (t1/2 = 4.5 h)-dependent manner. TPA (100 nM for 15 h) lowered the Bmax of [3H]STX binding by 53% without altering the KD value. Phorbol 12,13-dibutyrate (PDBu) also reduced [3H]STX binding, whereas 4α-TPA, an inactive analogue, had no effect. The inhibitory effect of TPA was abolished when H-7 (an inhibitor of PKC), but not H-89 (an inhibitor of cyclic AMP-dependent protein kinase), was included in the culture medium for 1 h before and during TPA treatment. Simultaneous treatment with TPA in combination with either actinomycin D or cycloheximide, an inhibitor of protein synthesis, nullified the effect of TPA. TPA treatment also attenuated veratridine-induced 22Na+ influx but did not alter the affinity of veratridine for Na channels as well as an allosteric potentiation of veratridine-induced 22Na+ influx by brevetoxin. These results suggest that an activation of PKC down-regulates the density of Na channels without altering their pharmacological features; this down-regulation is mediated via the de novo synthesis of an as yet unidentified protein(s), rather than an immediate effect of Na channel phosphorylation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.1996.66031249.x
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  • 2
    Electronic Resource
    Electronic Resource
    Proadrenomedullin N-Terminal 20 Peptide (PAMP), an Endogenous Anticholinergic Peptide: Its Exocytotic Secretion and Inhibition of Catecholamine Secretion in Adrenal Medulla (1995)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 64 (1995), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: In cultured bovine adrenal medullary cells, stimulation of nicotinic receptors by carbachol evoked the Ca2+-dependent exocytotic cosecretion of proadrenomedullin N-terminal 20 peptide (PAMP) (EC50 = 50.1 µM) and catecholamines (EC50 = 63.0 µM), with the molar ratio of PAMP/catecholamines secreted being equal to the ratio in the cells. Addition of PAMP[1–20]NH2 inhibited carbachol-induced 22Na+ influx via nicotinic receptors (IC50 = 2.5 µM) in a noncompetitive manner and thereby reduced carbachol-induced 45Ca2+ influx via voltage-dependent Ca2+ channels (IC50 = 1.0 µM) and catecholamine secretion (IC50 = 1.6 µM). It did not alter high K+-induced 45Ca2+ influx via voltage-dependent Ca2+ channels or veratridine-induced 22Na+ influx via voltage-dependent Na+ channels. PAMP seems to be a novel antinicotinic peptide cosecreted with catecholamines by a Ca2+-dependent exocytosis in response to nicotinic receptor stimulation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.1995.64010459.x
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  • 3
    Electronic Resource
    Electronic Resource
    Large- and small-conductance Ca2+-activated K+ channels: their role in the nicotinic receptor-mediated catecholamine secretion in bovine adrenal medulla (1995)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 352 (1995), S. 545-549 
    Details
    ISSN: 1432-1912
    Keywords: 86Rb+ efflux ; Charybdotoxin ; Iberiotoxin ; Apamin ; 45Ca2+ influx ; Catecholamine secretion ; Nicotinic receptors ; Adrenal chromaffln cell
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In cultured bovine adrenal chromaffln cells, charybdotoxin and iberiotoxin (inhibitors of the large-conductance Ca2+-activated K+ channel) as well as apamin (an inhibitor of the small-conductance Ca2+-activated K+ channel), at 1–100 nM, suppressed carbachol-induced 86Rb+ efflux, augmented carbachol-induced 45Ca2+ influx via voltage-dependent Ca2+ channels and catecholamine secretion and had no effect on carbachol-induced 22Na+ influx via nicotinic receptors, a prerequisite for Ca2+ channel activation by carbachol. 45Ca2+ influx caused by high K+ (a direct activation of voltage-dependent Ca2+ channels) was also enhanced by these K+ channel inhibitors, with the concentration-response curves being similar to those for carbachol-induced 45Ca2+ influx. Dendrotoxin and mast cell degranulating peptide (inhibitors of voltage-dependent K+ channels), on the other hand, did not alter carbachol-induced 86Rb+ efflux or 45Ca2+ influx. These results suggest that the stimulation of nicotinic receptors eventually opens large- and small-conductance Ca2+-activated K+ channels, and that the blockade of these Ca2+-activated K+ channels results in gating of voltage-dependent Ca2+ channels and thereby augments catecholamine secretion from bovine adrenal chromaffln cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00169389
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  • 4
    Electronic Resource
    Electronic Resource
    Large- and small-conductance Ca2+-activated KK+ channels: their role in the nicotinic receptor-mediated catecholamine secretion in bovine adrenal medulla (1995)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 352 (1995), S. 545-549 
    Details
    ISSN: 1432-1912
    Keywords: Key words 86Rb+ efflux ; Charybdotoxin ; Iberiotoxin ; Apamin ; 45Ca2+ influx ; Catecholamine secretion ; Nicotinic receptors ; Adrenal chromaffin cell
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  In cultured bovine adrenal chromaffin cells, charybdotoxin and iberiotoxin (inhibitors of the large-conductance Ca2+-activated K+ channel) as well as apamin (an inhibitor of the small-conductance Ca2+-activated K+ channel), at 1–100 nM, suppressed carbachol-induced 86Rb+ efflux, augmented carbachol-induced 45Ca2+ influx via voltage-dependent Ca2+ channels and catecholamine secretion and had no effect on carbachol-induced 22Na+ influx via nicotinic receptors, a prerequisite for Ca2+ channel activation by carbachol. 45Ca2+ influx caused by high K+ (a direct activation of voltage-dependent Ca2+ channels) was also enhanced by these K+ channel inhibitors, with the concentration-response curves being similar to those for carbachol-induced 45Ca2+ influx. Dendrotoxin and mast cell degranulating peptide (inhibitors of voltage-dependent K+ channels), on the other hand, did not alter carbachol-induced 86Rb+ efflux or 45Ca2+ influx. These results suggest that the stimulation of nicotinic receptors eventually opens large- and small-conductance Ca2+-activated K+ channels, and that the blockade of these Ca2+-activated K+ channels results in gating of voltage-dependent Ca2+ channels and thereby augments catecholamine secretion from bovine adrenal chromaffin cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00169389
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  • 5
    Electronic Resource
    Electronic Resource
    Functional relation between nitric oxide and noradrenaline for the modulation of vascular tone in rat mesenteric vasculature (1994)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 349 (1994), S. 362-366 
    Details
    ISSN: 1432-1912
    Keywords: Key words: Mesenteric vasculatur – Nitric oxide – Nv-Nitro-L-arginine – Noradrenaline – Vasoconstriction
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract. As previously reported, Nv-nitro-L-arginine (L-NNA), an inhibitor of nitric oxide (NO) synthesis, decreased transmural field stimulation (TFS)-induced noradrenaline overflow from the isolated perfused rat mesenteric vasculature attached to the intestine. The decrease was attenuated by L-arginine. This suggests that NO may increase noradrenaline release (Yamamoto et al. 1993).   The present experiments with this preparation were done in order to monitor changes in vascular perfusion pressure caused by TFS or by noradrenaline infusion in parallel with those in the noradrenaline outflow caused by TFS in the presence of atropine (0.1 μmol/l) (to block acetylcholine-induced release of endothelial NO) and of indomethacin (3 μmol/l) (to inhibit L-NNA-induced production of vasoconstrictor prostanoids). (1) TFS (2–10 Hz) caused a frequency-dependent increase in noradrenaline overflow and perfusion pressure. (2) L-NNA (10 and 30 μmol/l) caused a concentration-dependent inhibition of TFS-induced noradrenaline overflow, whereas the TFS-induced pressure increase was augmented by L-NNA in a concentration-dependent manner. At any given concentration of L-NNA, the potentiation of vasoconstriction by L-NNA became greater in magnitude as the frequency of the TFS was raised. (3) Infusion of noradrenaline (0.38–6 nmol) caused a dose-dependent increase in perfusion pressure up to a value comparable with that caused by TFS. The pressure increase in response to noradrenaline infusion was also enhanced by L-NNA, relatively, to a greater extent than the enhancement, by L-NNA, of the pressure response to TFS. (4) These effects of L-NNA were significantly attenuated by L-arginine (0.3 mmol/l) or sodium nitroprusside (1 μmol/l). Our results suggest that NO, presumably originating from several sites, may stimulate the release of noradrenaline in the mesenteric vasculature and that the consequent rise in circulating noradrenaline, in turn, causes the liberation of endothelial NO.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00170881
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  • 6
    Electronic Resource
    Electronic Resource
    Characterization of [3H]brevetoxin binding to voltage-dependent sodium channels in adrenal medullary cells (1994)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 350 (1994), S. 209-212 
    Details
    ISSN: 1432-1912
    Keywords: Key words: Adrenal chromaffin cells – Sodium channel – Binding – Brevetoxin – Veratridine – Scorpion venoms
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract. We have previously reported that in bovine adrenal chromaffin cells Ptychodiscus brevis toxin-3 (PbTx-3) does not alter the veratridine-induced 22Na influx when given alone, but increases the influx of 22Na when co-applied with either α- or β-scorpion venom (Wada et al. 1992). In the present study, we characterized [3H]PbTx-3 binding in bovine adrenal chromaffin cells. [3H]PbTx-3 binding was saturable, reversible and of high-affinity with an equilibrium dissociation constant (Kd) of 32.0±4.9 nmol/l and a maximum binding capacity (Bmax) of 6.2±1.2 pmol/4×106 cells (4.5±0.9 pmol/mg cell protein). A Hill plot revealed the lack of cooperative interaction among the binding sites. Unlabelled PbTx-3 inhibited [3H]PbTx-3 binding with an IC50 of 31 nmol/l. However, tetrodotoxin, veratridine, α- and β-scorpion venom, or veratridine in combination with either α- or β-scorpion venom did not alter [3H]PbTx-3 binding. All these results suggest that PbTx-3 binds to a site (site 5) distinct from the previously known four toxin binding sites, which does not gate voltage-dependent Na channels by itself, but is specifically involved in the allosteric modulation of Na channels in adrenal medullary cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00241098
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  • 7
    Electronic Resource
    Electronic Resource
    Nω-nitro-L-arginine, an inhibitor of nitric oxide synthesis, decreases noradrenaline outflow in rat isolated perfused mesenteric vasculature (1993)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 347 (1993), S. 238-240 
    Details
    ISSN: 1432-1912
    Keywords: Nω-Nitro-L -arginine ; Non-adrenergic, noncholinergic neurotransmission ; Noradrenaline overflow ; Nitric oxide ; Mesenteric vasculature
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In the isolated perfused rat mesenteric vasculature with intestine attached Nω-nitro-L-arginine (L- NNA) (30 μmol/l) an inhibitor of nitric oxide (NO) synthesis from L-arginine, did not alter spontaneous noradrenaline outflow. Transmural field stimulation (2–10 Hz) caused a frequency-dependent increase in noradrenaline outflow. The evoked overflow was reduced by L-NNA. L-Arginine (0.3 mmol/l) attenuated the inhibition of noradrenaline overflow by L-NNA. These results suggest that NO increases the release of noradrenaline in rat mesenteric vasculature.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00169274
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  • 8
    Electronic Resource
    Electronic Resource
    Characterization of [3H]brevetoxin binding to voltage-dependent sodium channels in adrenal medullary cells (1994)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 350 (1994), S. 209-212 
    Details
    ISSN: 1432-1912
    Keywords: Adrenal chromaffin cells ; Sodium channel ; Binding ; Brevetoxin ; Veratridine ; Scorpion venoms
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We have previously reported that in bovine adrenal chromaffin cells Ptychodiscus brevis toxin-3 (PbTx-3) does not alter the veratridine-induced 22Na influx when given alone, but increases the influx of 22Na when co-applied with either α- or β-scorpion venom (Wada et al. 1992). In the present study, we characterized [3H]PbTx-3 binding in bovine adrenal chromaffin cells. [3H]PbTx-3 binding was saturable, reversible and of high-affinity with an equilibrium dissociation constant (Kd) of 32.0±4.9 nmol/1 and a maximum binding capacity Bmax of 6.2 ± 1.2 pmol/4 × 106 cells (4.5 ± 0.9 pmol/mg cell protein). A Hill plot revealed the lack of cooperative interaction among the binding sites. Unlabelled PbTx-3 inhibited [3H]PbTx-3 binding with an IC50 of 31 nmol/l. However, tetrodotoxin, veratridine, α- and β-scorpion venom, or veratridine in combination with either α- or β-scorpion venom did not alter [3H]PbTx-3 binding. All these results suggest that PbTx-3 binds to a site (site 5) distinct from the previously known four toxin binding sites, which does not gate voltage-dependent Na channels by itself, but is specifically involved in the allosteric modulation of Na channels in adrenal medullary cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00241098
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  • 9
    Electronic Resource
    Electronic Resource
    Functional relation between nitric oxide and noradrenaline for the modulation of vascular tone in rat mesenteric vasculature (1994)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 349 (1994), S. 362-366 
    Details
    ISSN: 1432-1912
    Keywords: Mesenteric vasculatur ; Nitric oxide ; Nω-Nitro-l-arginine ; Noradrenaline ; Vasoconstriction
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract As previously reported, Nω-nitro-l-arginine (l-NNA), an inhibitor of nitric oxide (NO) synthesis, decreased transmural field stimulation (TFS)-induced noradrenaline overflow from the isolated perfused rat mesenteric vasculature attached to the intestine. The decrease was attenuated by l-arginine. This suggests that NO may increase noradrenaline release (Yamamoto et al. 1993). The present experiments with this preparation were done in order to monitor changes in vascular perfusion pressure caused by TFS or by noradrenaline infusion in parallel with those in the noradrenaline outflow caused by TFS in the presence of atropine (0.1 μmol/l) (to block acetylcholine-induced release of endothelial NO) and of indomethacin (3 μmol/l) (to inhibit l-NNA-induced production of vasoconstrictor prostanoids). (1) TFS (2–10 Hz) caused a frequency-dependent increase in noradrenaline overflow and perfusion pressure. (2) l-NNA (10 and 30 μmol/l) caused a concentration-dependent inhibition of TFS-induced noradrenaline overflow, whereas the TFS-induced pressure increase was augmented by l-NNA in a concentration-dependent manner. At any given concentration of l-NNA, the potentiation of vasoconstriction by l-NNA became greater in magnitude as the frequency of the TFS was raised. (3) Infusion of noradrenaline (0.38–6 nmol) caused a dose-dependent increase in perfusion pressure up to a value comparable with that caused by TITS. The pressure increase in response to noradrenaline infusion was also enhanced by l-NNA, relatively, to a greater extent than the enhancement, by l-NNA, of the pressure response to TFS. (4) These effects of l-NNA were significantly attenuated by l-arginine (0.3 mmol/l) or sodium nitroprusside (1 μmol/l). Our results suggest that NO, presumably originating from several sites, may stimulate the release of noradrenaline in the mesenteric vasculature and that the consequent rise in circulating noradrenaline, in turn, causes the liberation of endothelial NO.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00170881
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