Nicotine-induced release of noradrenaline and neuropeptide Y in guinea-pig heart: role of calcium channels and protein kinase C

Author(s):  
Markus Haass ◽  
Gert Richardt ◽  
homas Brenn ◽  
Edgar Sch�mig ◽  
Albert Sch�mig
1990 ◽  
Vol 259 (5) ◽  
pp. R925-R930
Author(s):  
M. Haass ◽  
C. Forster ◽  
G. Richardt ◽  
R. Kranzhofer ◽  
A. Schomig

The role of calcium for the release of norepinephrine (NE, determined by high-pressure liquid chromatography) and neuropeptide Y (NPY, determined by radioimmunoassay) was investigated in guinea pig perfused hearts with intact sympathetic innervation. In the presence of extracellular calcium (1.85 mM), electrical stimulation of the left stellate ganglion (12 Hz, 1 min) induced a closely related release of NE and NPY with the molar ratio of approximately 400-600 (NE) to 1 (NPY). The stimulation-evoked overflow of both transmitters was dependent from the extracellular calcium concentration and was almost completely suppressed by calcium-free perfusion. The corelease of both transmitters was not affected by the L-type calcium channel blocker felodipine (1-10 microM). However, the overflow of NE and NPY was markedly attenuated by the unselective calcium antagonist flunarizine (1-10 microM) and completely prevented by the neuronal (N-type) calcium channel blockers omega-conotoxin (1-100 nM) and cadmium chloride (10-100 microM), indicating a key role for N-type calcium channels in the exocytotic release of transmitters from cardiac sympathetic nerve fibers. Possibly due to unspecific actions, such as interference with sodium channels or uptake1-blocking properties, the phenylalkylamines verapamil (0.01-10 microM) and gallopamil (1-10 microM) reduced NPY overflow with only a minor effect on NE overflow. The stimulation-induced transmitter release was increased up to twofold by activation of protein kinase C (phorbol 12-myristate 13-acetate, 3 nM-3 microM) and completely suppressed by inhibition of protein kinase C (polymyxin B, 100 microM).(ABSTRACT TRUNCATED AT 250 WORDS)


2012 ◽  
Vol 53 (6) ◽  
pp. 2904 ◽  
Author(s):  
Luke B. Potts ◽  
Yi Ren ◽  
Guangrong Lu ◽  
Enoch Kuo ◽  
Ellen Ngo ◽  
...  

Pharmacology ◽  
1996 ◽  
Vol 53 (1) ◽  
pp. 60-65 ◽  
Author(s):  
H.S. Odes ◽  
R. Reimer ◽  
R. Muallem ◽  
M. Schwenk ◽  
W. Beil ◽  
...  

1997 ◽  
Vol 74 (2) ◽  
pp. 155-163 ◽  
Author(s):  
Noriko Saitoh ◽  
Ritsuko Fujimoto ◽  
Toshiaki Ishii ◽  
Hideaki Nishio ◽  
Tadayoshi Takeuchi ◽  
...  

1994 ◽  
Vol 39 (12) ◽  
pp. 2547-2557 ◽  
Author(s):  
Naotsuka Okayama ◽  
Takashi Joh ◽  
Tadahisa Miyamoto ◽  
Taiji Kato ◽  
Makoto Itoh

1987 ◽  
Vol 253 (5) ◽  
pp. H1321-H1324 ◽  
Author(s):  
N. Tohse ◽  
M. Kameyama ◽  
H. Irisawa

Effects of protein kinase C (PKC) and intracellular calcium ion (Cai2+) on the delayed rectifier K+ current (IK) were investigated in the single ventricular cells of guinea pig by use of an internal-dialysis method and a whole cell voltage-clamp technique. 12-O-tetradecanoylphorbol-13-acetate (TPA, 10(-9) M), an activator of PKC, increased the amplitude of IK in the presence of Cai2+ higher than 10(-10) M. This effect of TPA was mimicked by a synthetic diacylglycerol, 1-oleoyl-2-acetylglycerol (OAG), 50 micrograms/ml, 125 microM, and was blocked by 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine (10 microM). The above findings suggest that IK channels were phosphorylated by PKC and thereby the amplitude of IK was increased. IK was also increased by elevating the concentration of Cai2+ in the absence of TPA. It is thus indicated that IK channels are modulated by Cai2+ not only through activation of PKC but also directly. Our observation may provide a possible mechanism by which Cai2+ mediates the link between the Ca2+ transients during contraction and the action potential duration.


1997 ◽  
Vol 74 (2) ◽  
pp. 155-163
Author(s):  
Noriko Saitoh ◽  
Ritsuko Fujimoto ◽  
Toshiaki Ishii ◽  
Hideaki Nishio ◽  
Tadayoshi Takeuchi ◽  
...  

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