Role of Potassium Channels in the GABA Inhibitory Action on the Purinergic Response to Electrical Field Stimulation in Rat Isolated Vas Deferens

1999 ◽  
Vol 5 (6) ◽  
pp. 407-409
Author(s):  
V. Calderone ◽  
B. Baragatti ◽  
S. Rossi ◽  
P. Nieri ◽  
E. Martinotti
Keyword(s):  
Potassium Channels ◽  
Inhibitory Action ◽  
Vas Deferens ◽  
Electrical Field Stimulation ◽  
Field Stimulation ◽  
Electrical Field

Release of epithelium-derived PGE2 from canine trachea after antigen inhalation

1998 ◽  
Vol 274 (2) ◽  
pp. L220-L225 ◽  
Author(s):  
I. McGrogan ◽  
L. J. Janssen ◽  
J. Wattie ◽  
P. M. O’Byrne ◽  
E. E. Daniel
Keyword(s):  
Smooth Muscle ◽  
Electrical Field Stimulation ◽  
Tracheal Smooth Muscle ◽  
Organ Bath ◽  
Field Stimulation ◽  
Electrical Field ◽  
Concentration Response Curve

To investigate the role of prostaglandin (PG) E2 in allergen-induced hyperresponsiveness, dogs inhaled either the allergen Ascaris suum or vehicle (Sham). Twenty-four hours after inhalation, some animals exposed to allergen demonstrated an increased responsiveness to acetylcholine challenge in vivo (Hyp-Resp), whereas others did not (Non-Resp). Strips of tracheal smooth muscle, either epithelium intact or epithelium denuded, were suspended on stimulating electrodes, and a concentration-response curve to carbachol (10−9 to 10−5 M) was generated. Tissues received electrical field stimulation, and organ bath fluid was collected to determine PGE2content. With the epithelium present, all three groups contracted similarly to 10−5 M carbachol, whereas epithelium-denuded tissues from animals that inhaled allergen contracted more than tissues from Sham dogs. In response to electrical field stimulation, Hyp-Resp tissues contracted less than Sham tissues in the presence of epithelium and more than Sham tissues in the absence of epithelium. PGE2release in the muscle bath was greater in Non-Resp tissues than in Sham or Hyp-Resp tissues when the epithelium was present. Removal of the epithelium greatly inhibited PGE2release. We conclude that tracheal smooth muscle is hyperresponsive in vitro after in vivo allergen exposure only when the modulatory effect of the epithelium, largely through PGE2 release, is removed.

scholarly journals Role of cAMP and neuronal K+channels on α2-AR-induced inhibition of ACh release in equine trachea

1998 ◽  
Vol 274 (5) ◽  
pp. L827-L832
Author(s):  
Xiang-Yang Zhang ◽  
Feng-Xia Zhu ◽  
N. Edward Robinson
Keyword(s):  
Electrical Field Stimulation ◽  
Intracellular Camp ◽  
Field Stimulation ◽  
Ach Release ◽  
Electrical Field ◽  
K Channels ◽  
Parasympathetic Nerves ◽  
Pathway Activation ◽  
Before And After

To investigate the effects of changes in intracellular cAMP on α2-adrenoceptor (AR)-induced inhibition of airway acetylcholine (ACh) release, we examined the effects of the α2-AR agonist clonidine on electrical field stimulation-evoked ACh release from equine tracheal parasympathetic nerves before and after treatment with 8-bromo-cAMP or forskolin. We also tested whether charybdotoxin (ChTX)- or iberiotoxin (IBTX)-sensitive Ca2+-activated K+ channels mediate α2-AR-induced inhibition by examining the effect of clonidine in the absence and presence of ChTX or IBTX on ACh release. The amount of released ACh was measured by HPLC coupled with electrochemical detection. Clonidine (10−7 to 10−5 M) dose dependently inhibited ACh release before and after treatment with 8-bromo-cAMP (10−3 M) or forskolin (3 × 10−5M). ChTX and IBTX, both at the concentration of 5 × 10−7 M, significantly increased ACh release; however, they did not alter the magnitude of clonidine-induced inhibition. These results indicated that in equine tracheal parasympathetic nerves, α2-AR-induced inhibition of ACh release is via an intracellular cAMP-independent pathway. Activation of both ChTX- and IBTX-sensitive Ca2+-activated K+ channels inhibits the electrical field stimulation-evoked ACh release, but these channels are not involved in the α2-AR-induced inhibition of ACh release.

Evaluation of Antidepressant Effects on Recovery of Electrical Field Stimulation-Induced Contractions that have been Suppressed by Clonidine in Isolated Rat Vas Deferens

Pharmacology ◽  
2019 ◽  
Vol 103 (3-4) ◽  
pp. 189-201
Author(s):  
Keisuke Obara ◽  
Mayumi Michino ◽  
Masataka Ito ◽  
Lin Ao ◽  
Ayano Sawada ◽  
...  
Keyword(s):  
Receptor Antagonist ◽  
Tricyclic Antidepressants ◽  
Vas Deferens ◽  
Electrical Field Stimulation ◽  
Rat Vas Deferens ◽  
Blood Levels ◽  
Field Stimulation ◽  
Electrical Field ◽  
Tetracyclic Antidepressant ◽  
Isolated Rat

Background: A report examining whether clinically available antidepressants increase urethral smooth muscle contraction via antagonistic effects on the α2-adrenoceptor (α2-AR) is lacking. Objectives: The present study was performed to evaluate the potential of clinically available antidepressants to reverse α2-AR-mediated contractile inhibition in rat vas deferens, in order to predict whether they can induce voiding impairment. Method: The effects of 18 antidepressants of different classes on electrical field stimulation (EFS)-induced contractions suppressed by 10–8 mol/L clonidine (a selective α2-AR agonist) in isolated rat vas deferens were investigated and related to their respective clinical blood concentrations. Results: The EFS-induced contractions suppressed by clonidine were recovered by amitriptyline (a tricyclic antidepressant), mirtazapine (a noradrenergic and specific serotonergic antidepressant), and trazodone (a serotonin 5-HT2A receptor antagonist) at concentrations close to the clinical blood levels. EFS-induced contractions were also recovered by trimipramine, clomipramine (tricyclic antidepressants), mianserin (a tetracyclic antidepressant), sertraline (a selective serotonin reuptake inhibitor [SSRI]), and sulpiride (a dopamine D2-receptor antagonist), albeit at concentrations that substantially exceeded their clinically-achievable blood levels. EFS-induced contractions were not significantly affected by imipramine, nortriptyline, amoxapine (tricyclic antidepressants), maprotiline (a tetracyclic antidepressant), fluvoxamine, paroxetine, escitalopram (SSRIs), milnacipran, duloxetine (serotonin and noradrenaline reuptake inhibitors), and aripiprazole (a dopamine partial agonist). Conclusions: These findings suggest that amitriptyline, mirtazapine, and trazodone induce voiding impairment caused by increased urethral resistance by enhancing sympathetic nerve activities attributed to α2-AR antagonism.

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