CONTRACTILE RESPONSES OF PROSTATIC AND EPIDIDYMAL PORTIONS OF ISOLATED RABBIT VAS DEFERENS TO ELECTRICAL FIELD STIMULATION

Contractile responses of canine tracheal smooth muscle to electrical field stimulation diminished over a 2-h period of incubation. However, addition of indomethacin (10(-5) M) for a similar time not only prevented this inhibition of contractile response, but actually markedly increased the response to electrical field stimulation, suggesting that prostaglandins were responsible for the time-dependent inhibition. Measured prostaglandin E2 increased in the tissue bath over 2 h in control tissues. Addition of prostaglandin E2 to the tissue produced similar inhibition of contractile responses to electrical field stimulation in a concentration-dependent manner. In contrast, incubation alone, treatment with indomethacin, or addition of prostaglandin E2 had little, if any, effect on contractions induced by acetylcholine. We conclude that the release of prostaglandins from canine tracheal smooth muscle that occurs with time has a predominantly inhibitory effect on cholinergic neurotransmission at a prejunctional site.

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The effects of hydrogen sulfide on electrical field stimulation-induced neurogenic contractile responses in isolated rabbit lower esophageal sphincter: Contribution of nitrergic and non-adrenergic non-cholinergic transmission

Pharmacological Reports ◽

10.1016/j.pharep.2016.09.007 ◽

2016 ◽

Vol 68 (6) ◽

pp. 1350-1357

Author(s):

Halil Kara ◽

Fatma Isli ◽

Gokce Sevim Ozturk Fincan ◽

Seniz Yildirim ◽

Sevim Ercan ◽

...

Keyword(s):

Hydrogen Sulfide ◽

Lower Esophageal Sphincter ◽

Electrical Field Stimulation ◽

Field Stimulation ◽

Cholinergic Transmission ◽

Electrical Field ◽

Contractile Responses ◽

Esophageal Sphincter

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768Piboserod antagonizes serotonin (5-HT) potentiation of cholinergic contractile responses to electrical field stimulation in human detrusor muscle

European Urology Supplements ◽

10.1016/s1569-9056(05)80772-9 ◽

2005 ◽

Vol 4 (3) ◽

pp. 194

Author(s):

B. Darblade ◽

D. Behr-Roussel ◽

D. Gomy ◽

T. Lehret ◽

G. Benoit ◽

...

Keyword(s):

Electrical Field Stimulation ◽

Detrusor Muscle ◽

Field Stimulation ◽

Electrical Field ◽

Contractile Responses ◽

Human Detrusor

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Nitric oxide enhances contractile response of guinea-pig vas deferens to electrical field stimulation

The Japanese Journal of Pharmacology ◽

10.1016/s0021-5198(19)48352-2 ◽

2000 ◽

Vol 82 ◽

pp. 222

Author(s):

Hironori Nakanishi ◽

Takako Chiba ◽

Tomoyuki Ono ◽

Isao Matsuoka

Keyword(s):

Nitric Oxide ◽

Guinea Pig ◽

Vas Deferens ◽

Contractile Response ◽

Electrical Field Stimulation ◽

Field Stimulation ◽

Electrical Field

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

Pharmacology ◽

10.1159/000495616 ◽

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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