scholarly journals Role of K+ channels in the modulation of cholinergic neural responses in guinea-pig and human airways.

1992 ◽  
Vol 455 (1) ◽  
pp. 1-15 ◽  
Author(s):  
M Miura ◽  
M G Belvisi ◽  
C D Stretton ◽  
M H Yacoub ◽  
P J Barnes
2018 ◽  
Vol 818 ◽  
pp. 30-37 ◽  
Author(s):  
Ken Lee ◽  
Ayu Isogai ◽  
Minori Antoh ◽  
Shunichi Kajioka ◽  
Masatoshi Eto ◽  
...  

1992 ◽  
Vol 73 (6) ◽  
pp. 2505-2510 ◽  
Author(s):  
M. G. Belvisi ◽  
C. D. Stretton ◽  
M. Miura ◽  
G. M. Verleden ◽  
S. Tadjkarimi ◽  
...  

Inhibitory nonadrenergic noncholinergic (i-NANC) nerves are the only neural bronchodilator pathway in human airways. Possible candidates for the neurotransmitter include vasoactive intestinal peptide (VIP) and nitric oxide (NO) and purines such as ATP. We have investigated the potential role of these neurotransmitters. Phosphoramidon (10(-5) M) significantly potentiated relaxations to low doses of VIP with no effect on i-NANC responses. Relaxations induced by VIp were abolished with alpha-chymotrypsin (2 U/ml), but i-NANC responses were unaffected. Reactive blue 2 had no effect on i-NANC neural responses, indicating that endogenous ATP was not involved. The NO synthase inhibitor L-NG-nitroarginine methyl ester (L-NAME, 10(-4) M) produced a concentration-dependent inhibition of the i-NANC response, producing almost complete inhibition at every frequency studied (0.5–40 Hz), whereas L-NG-monomethyl arginine was effective only at low stimulation frequencies. The inhibitory effect of L-NAME was partially reversed by L- but not D-arginine, and D-NAME was without effect. These results suggest that in human tracheal segments the neural bronchodilator response is mediated by NO, and there is no functional evidence for implicating VIP in this response.


1994 ◽  
Vol 266 (6) ◽  
pp. L698-L704
Author(s):  
D. G. Baker ◽  
H. F. Don ◽  
J. K. Brown

Our goals were to establish that an alpha 2-adrenergic agonist (clonidine) inhibits ACh release from airway nerve endings and to test effects of iberiotoxin (IBTX), an inhibitor of fast-conductance, Ca(2+)-activated K+ channels on alpha 2-adrenergic and muscarinic attenuation of ACh release. Guinea pig tracheas were mounted between electrodes in buffer containing indomethacin and neostigmine, and high-performance liquid chromatography with electrochemical detection was used to measure ACh release during electrical field stimulation. Clonidine inhibited ACh release in a concentration-dependent fashion [maximum reduction: 48 +/- 3%; 50% inhibitory constant (IC50): 0.1 microM], and idazoxan, alpha 2-adrenergic antagonist, reversed the effect. However, IBTX failed to alter clonidine-induced attenuation of ACh release. In contrast, IBTX did cause an increase in tracheal tension. In addition, IBTX failed to reverse any of the potent autoinhibitory effects of endogenous ACh. Our results confirm the presence of inhibitory alpha 2-adrenergic receptors. However, activation of IBTX-sensitive K+ channels does not appear necessary for either alpha 2-adrenergic or muscarinic cholinergic inhibition of ACh release.


1999 ◽  
Vol 19 (2) ◽  
pp. 182-187
Author(s):  
Kazushi Tamai ◽  
Hikaru Suzuki ◽  
Shoichiro Shirai ◽  
Yuichiro Ogura
Keyword(s):  

2003 ◽  
Vol 284 (3) ◽  
pp. G392-G398 ◽  
Author(s):  
Edward Parr ◽  
Maria J. Pozo ◽  
Burton Horowitz ◽  
Mark T. Nelson ◽  
Gary M. Mawe

The current study was undertaken to test the existence and possible role of ether-a-go-go-related gene 1 (ERG1) protein K+ channels in gallbladder smooth muscle (GBSM). Transcripts encoding ERG1 were detected in human, mouse, and guinea pig GBSM, and ERG1 immunoreactivity was observed in GBSM cells. In intracellular voltage recordings, addition of E-4031 (100 nM–1 μM) or cisapride (100 nM–2 μM) caused concentration-dependent excitation of guinea pig GBSM that was not affected by 500 nM TTX + 5 μM atropine, and E-4031 also depolarized the resting membrane potential. In muscle strip studies, E-4031 either induced phasic contractions or significantly increased the amplitude of phasic contractions in spontaneously active tissues ( P = 0.001). E-4031 also potentiated bethanechol-induced contractions. In conclusion, ERG1 channels are expressed in the GBSM, where they play a role in excitation-contraction coupling probably by contributing to repolarization of the plateau phase of the action potential and to the resting membrane potential.


2004 ◽  
Vol 142 (7) ◽  
pp. 1105-1114 ◽  
Author(s):  
Bin-Nan Wu ◽  
Rong-Jyh Lin ◽  
Yi-Ching Lo ◽  
Kuo-Pyng Shen ◽  
Chao-Chuan Wang ◽  
...  

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