Article date: October 1993
By: Kiyohisa Sekizawa, Takeyasu Fukushima, Yasushi Ikarashi, Yuji Maruyama, Hidetada Sasaki, in Volume 110, Issue 2, pages 816-820
We have investigated the role of nitric oxide (NO) in cholinergic contraction in rat trachea.
Methylene blue (10 nm to 30 μm) potentiated cholinergic contraction induced by electrical field stimulation (EFS) at 5 Hz in a concentration‐dependent fashion. At a concentration of 30 μm, methylene blue decreased responses to log EFS frequency, producing 50% of maximum contraction from a control value of 0.74 ± 0.09 Hz to 0.30 ± 0.05 Hz without a significant effect on concentration‐response curves to acetylcholine (ACh).
NG‐monomethyl‐l‐arginine (l‐NMMA; 100 μm) also potentiated cholinergic contraction induced by EFS at 5 Hz (131.5 ± 4.6% of control) without having any effect against ACh (3 μm)‐induced contractions. Likewise, l‐NMMA (100 μm) significantly increased EFS (5 Hz)‐evoked release of ACh from tracheal segments into the bath solution (51.4 ± 4.0 pmol ml−1 in the presence of l‐NMMA and 35.0 ± 1.8 pmol ml−1 in the absence of l‐NMMA, respectively).
Administration of NO (present in acidified soluton of NaNO2) (1 nm to 10 μm) and sodium nitroprusside (100 nm to 10 μm) concentration‐dependently reduced EFS (5 Hz)‐induced cholinergic contractions without having a significant effect on ACh (3 μm)‐induced contractions. These results were unaffected by prior exposure of the tissues to l‐NMMA (100 μm).
Dibutyryl cyclic GMP (3 mm) also reduced cholinergic contractions induced by EFS at 5 Hz (70.1 ± 3.6% of control) without any significant effect on ACh (3 μm)‐induced contractions.
Pretreatment of tissues with capsaicin (30 μm) or α‐chymotrypsin (1 u ml−1) failed to inhibit methylene blue (30 μm)‐induced potentiation of responses to EFS at 5 Hz.
These results suggest that an endogenous NO‐like factor may mediate prejunctional inhibition of cholinergic contraction through a cyclic GMP‐dependent mechanism in rat trachea.
We have investigated the role of nitric oxide (NO) in cholinergic contraction in rat trachea.
Methylene blue (10 nm to 30 μm) potentiated cholinergic contraction induced by electrical field stimulation (EFS) at 5 Hz in a concentration‐dependent fashion. At a concentration of 30 μm, methylene blue decreased responses to log EFS frequency, producing 50% of maximum contraction from a control value of 0.74 ± 0.09 Hz to 0.30 ± 0.05 Hz without a significant effect on concentration‐response curves to acetylcholine (ACh).
NG‐monomethyl‐l‐arginine (l‐NMMA; 100 μm) also potentiated cholinergic contraction induced by EFS at 5 Hz (131.5 ± 4.6% of control) without having any effect against ACh (3 μm)‐induced contractions. Likewise, l‐NMMA (100 μm) significantly increased EFS (5 Hz)‐evoked release of ACh from tracheal segments into the bath solution (51.4 ± 4.0 pmol ml−1 in the presence of l‐NMMA and 35.0 ± 1.8 pmol ml−1 in the absence of l‐NMMA, respectively).
Administration of NO (present in acidified soluton of NaNO2) (1 nm to 10 μm) and sodium nitroprusside (100 nm to 10 μm) concentration‐dependently reduced EFS (5 Hz)‐induced cholinergic contractions without having a significant effect on ACh (3 μm)‐induced contractions. These results were unaffected by prior exposure of the tissues to l‐NMMA (100 μm).
Dibutyryl cyclic GMP (3 mm) also reduced cholinergic contractions induced by EFS at 5 Hz (70.1 ± 3.6% of control) without any significant effect on ACh (3 μm)‐induced contractions.
Pretreatment of tissues with capsaicin (30 μm) or α‐chymotrypsin (1 u ml−1) failed to inhibit methylene blue (30 μm)‐induced potentiation of responses to EFS at 5 Hz.
These results suggest that an endogenous NO‐like factor may mediate prejunctional inhibition of cholinergic contraction through a cyclic GMP‐dependent mechanism in rat trachea.
DOI: 10.1111/j.1476-5381.1993.tb13885.x
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