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  • 1
    Electronic Resource
    Electronic Resource
    Possible Involvement of Hypothyroidism as a Cause of Lithium-Induced Sinus Node Dysfunction (1999)
    Oxford, UK : Blackwell Publishing Ltd
    Pacing and clinical electrophysiology 22 (1999), S. 0 
    Details
    ISSN: 1540-8159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Although several reports have stated that even therapeutic levels of lithium can induce sinus node dysfunction, the mechanism has not been fully elucidated. We present here two patients with sinus node dysfunction after long-term lithium therapy. Following lithium discontinuation, sinus node function recovered completely. After resuming lithium, however, irreversible sinus node dysfunction recurred and a permanent pacemaker was implanted in one patient. The serum concentration of lithium was within therapeutic levels. Nevertheless, hypothyroidism was associated with the sinus node dysfunction in both patients. Thus, thyroid function may play an important role in sinus node dysfunction induced by lithium. (PACE 1999; 22[Pt. I]-.954-957) lithium, sinus node dysfunction, hypothyroidism, sick sinus syndrome
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1540-8159.1999.tb06823.x
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  • 2
    Electronic Resource
    Electronic Resource
    Veratridine causes the Ca2+-dependent increase in diacylglycerol formation and translocation of protein kinase C to membranes in cultured bovine adrenal medullary cells (1992)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 346 (1992), S. 76-81 
    Details
    ISSN: 1432-1912
    Keywords: Amiloride ; Calcium ; Diacylglycerol ; Protein kinase C ; Veratridine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Our previous studies suggested that protein kinase C is involved in the veratridine (an activator of voltage-dependent Na+ channels)-induced phosphorylation and activation of tyrosine hydroxylase as well as the synthesis of catecholamines in adrenal medulla (Uezono et al. 1989). In the present study, we investigated whether treatment of cultured bovine adrenal medullary cells with veratridine causes the accumulation of diacylglycerol, a physiological activator of protein kinase C and the translocation of protein kinase C from cytosol to membrane, a process required for protein kinase C activation. Veratridine (100 μmol/l) increased diacylglycerol level about 2.2 fold in a monophasic manner, with peaking at 5 min and declining toward the basal level within 20 min. Veratridine also increased membrane protein kinase C from 15.6% to 26.9% of total protein kinase C in a timecourse similar to that of diacylglycerol accumulation. Both stimulatory effects of veratridine were inhibited by tetrodotoxin and not observed in Ca2+-free, EGTA-containing medium. Amiloride, an inhibitor of Na+/Ca2+ and Na+/H+ exchange, did not alter veratridine-induced events. These results suggest that veratridine-induced Ca2+ influx contributes to the accumulation of diacylglycerol and the activation of protein kinase C in adrenal medullary cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00167574
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Stimulatory effects of brain natriuretic peptide on cyclic GMP accumulation and tyrosine hydroxylase activity in cultured bovine adrenal medullary cells (1991)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 343 (1991), S. 289-295 
    Details
    ISSN: 1432-1912
    Keywords: Adrenal medulla ; Atrial natriuretic peptide ; Brain natriuretic peptide ; Cyclic GMP ; Tyrosine hydroxylase
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We studied the effect of brain natriuretic peptide (BNP) on the accumulation of cyclic GMP and the phosphorylation and activity of tyrosine hydroxylase, compared with that of atrial natriuretic peptide (ANP), in cultured bovine adrenal medullary cells. 1. BNP as well as ANP increased cellular cyclic GMP accumulation in a concentration-dependent manner (10–1000 nmol/1). BNP (1 μmol/1) and ANP (1 μmol/1) produced a 60-fold and 30-fold increase in cyclic GMP accumulation, respectively. 2. The stimulatory effects of BNP and ANP on cyclic GMP accumulation were observed even when Ca2+ or Na+ was removed from the incubation medium. 3. 12-O-Tetradecanoylphorbol 13-acetate (TPA), an activator of protein kinase C, inhibited the stimulatory effect of BNP on cyclic GMP accumulation in a concentration-dependent manner (1–100 nmol/1). Furthermore, the BNP-induced accumulation of cyclic GMP was attenuated by forskolin (1 μmol/1), an activator of adenylate cyclase. 4. BNP (1 μmol/1) and ANP (1 μ mol/1) caused a significant increase in phosphorylation and activity of tyrosine hydroxylase in the cells. 5. In digitonin-permeabilized cells, cyclic GMP (1–100 μmol/1) activated tyrosine hydroxylase in the presence of ATP and Mg2+. These results suggest that BNP stimulates the accumulation of cyclic GMP in a manner similar to that of ANP. The increased accumulation of cyclic GMP by these peptides may be negatively modulated by protein kinase C and cyclic AMP and may cause the phosphorylation and activation of tyrosine hydroxylase-in cultured bovine adrenal medullary cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00251128
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  • 4
    Electronic Resource
    Electronic Resource
    An active metabolite of carbamazepine, carbamazepine-10,11-epoxide, inhibits ion channel-mediated catecholamine secretion in cultured bovine adrenal medullary cells (1998)
    Springer
    Psychopharmacology 135 (1998), S. 368-373 
    Details
    ISSN: 1432-2072
    Keywords: Key words Carbamazepine-10 ; 11-epoxide ; Carbamazepine-10 ; 11-diol ; Catecholamine secretion ; Nicotinic acetylcholine receptor-associated ion channel ; Voltage-dependent Na+ channel ; N-type voltage-dependent Ca2+ channel
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  We have recently reported inhibitory effects of carbamazepine (CBZ) on ion channel-mediated secretion of catecholamines in bovine adrenal medullary cells. Here, we report the effects of carbamazepine-10,11-epoxide (CBZ-E), an active metabolite of CBZ, and carbamazepine-10,11-diol (CBZ-D), a non-active metabolite, on 22Na+ influx, 45Ca2+ influx and catecholamine secretion in cultured adrenal medullary cells. CBZ-E, but not CBZ-D inhibited 22Na+ influx, 45Ca2+ influx and catecholamine secretion induced by carbachol or veratridine with a half-maximal inhibitory concentration (IC50) of 0.26 or 0.68 μg/ml, respectively. CBZ-E also inhibited high K+-evoked 45Ca2+ influx and catecholamine secretion (IC50 = 0.3 μg/ml), but CBZ-D did not. These findings suggest that CBZ-E, but not CBZ-D, attenuates catecholamine secretion by inhibiting nicotinic acetylcholine receptor-associated ion channels, voltage-dependent Na+ channels and voltage-dependent Ca2+ channels in the cells. This inhibition of CBZ-E as well as CBZ may be related to the clinical effects in neuropsychiatric disorders.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002130050524
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  • 5
    Electronic Resource
    Electronic Resource
    Inhibition by carbamazepine of various ion channels-mediated catecholamine secretion in cultured bovine adrenal medullary cells (1995)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 352 (1995), S. 297-303 
    Details
    ISSN: 1432-1912
    Keywords: Key words: Adrenal medullary cells ; Carbamazepine ; Nicotinic acetylcholine receptor-associated ion channel ; Voltage-dependent Na+ channel ; Voltage-dependent Ca2+ channel
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  The effects of carbamazepine (CBZ) on 22Na+ influx, 45Ca2+ influx, catecholamine secretion and cyclic GMP production were examined in cultured bovine adrenal medullary cells. 1) CBZ (40–120 μmol/l) inhibited 22Na+ influx evoked by carbachol in a concentration-dependent manner. CBZ inhibited carbachol-evoked 45Ca2+ influx and catecholamine secretion at concentrations similar to those which suppressed 22Na+ influx. 2) CBZ (4–120 μmol/l) inhibited veratridine-induced 22Na+ influx, 45Ca2+ influx and catecholamine secretion. 3) CBZ (12 or 40–120 μmol/l) suppressed 56 mmol/l K+-evoked 45Ca2+ influx and catecholamine secretion, respectively. 4) Combination of CBZ with nitrendipine or ω-agatoxin-IVA produced further inhibition of 56 mmol/l K+- evoked 45Ca2+ influx and catecholamine secretion, compared to the effect of CBZ alone, whereas CBZ plus ω-conotoxin-GVIA did not produce any further inhibition. 5) CBZ (40 μmol/l) attenuated the production of cyclic GMP caused by muscarine. These results suggest that CBZ at therapeutic concentrations (16–48 μmol/l: 4–12 μg/ml) inhibits catecholamine secretion by interfering with nicotinic acetylcholine receptor-associated ion channels, voltage-dependent Na+ channels and N-type voltage-dependent Ca2+ channels, and may have an antimuscarinic effect in adrenal medullary cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00168560
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  • 6
    Electronic Resource
    Electronic Resource
    Inhibition by carbamazepine of various ion channels-mediated catecholamine secretion in cultured bovine adrenal medullary cells (1995)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 352 (1995), S. 297-303 
    Details
    ISSN: 1432-1912
    Keywords: Adrenal medullary cells ; Carbamazepine ; Nicotinic acetylcholine receptor-associated ion channel ; Voltage-dependent Na+ channel ; Voltage-dependent Ca2+ channel
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effects of carbamazepine (CBZ) on 22Na+ influx, 45Ca2+ influx, catecholamine secretion and cyclic GMP production were examined in cultured bovine adrenal medullary cells. 1 CBZ (40–120 μmol/l) inhibited 22Na+ influx evoked by carbachol in a concentration-dependent manner. CBZ inhibited carbachol-evoked 45Ca2+ influx and catecholamine secretion at concentrations similar to those which suppressed 22Na+ influx. 2 CBZ (4–120 μmol/l) inhibited veratridine-induced 22Na+ influx, 45Ca2+ influx and catecholamine secretion. 3 CBZ (12 or 40–120 μmol/l) suppressed 56 mmol/1 K+-evoked 45Ca2+ influx and catecholamine secretion, respectively. 4 Combination of CBZ with nitrendipine or ω-agatoxin-IVA produced further inhibition of 56 mmol/l K+ - evoked 45Ca2+ influx and catecholamine secretion, compared to the effect of CBZ alone, whereas CBZ plus ω-conotoxin-GVIA did not produce any further inhibition. 5 CBZ (40 μmol/1) attenuated the production of cyclic GMP caused by muscarine. These results suggest that CBZ at therapeutic concentrations (16–48 μmol/l: 4–12 μg/ml) inhibits catecholamine secretion by interfering with nicotinic acetylcholine receptor-associated ion channels, voltage-dependent Na+ channels and N-type voltage-dependent Ca2+ channels, and may have an antimuscarinic effect in adrenal medullary cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00168560
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    Paper (German National Licenses)
    Fulltext
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