The Effect of Caesium on Adrenergic Transmission in Rabbit Vas Deferens

1975 ◽  
Vol 53 (3) ◽  
pp. 410-415 ◽  
Author(s):  
A. Johns ◽  
D. M. Paton
Keyword(s):  
Vas Deferens ◽  
Contractile Response ◽  
Nerve Impulse ◽  
Prostaglandin Synthesis ◽  
Secondary Response ◽  
Neuronal Uptake ◽  
Transmural Stimulation ◽  
Adrenergic Transmission ◽  
Uptake Of Noradrenaline ◽  
Rabbit Vas Deferens

The effect of caesium on the responses of rabbit vas deferens to transmural stimulation was investigated. The tissue responded to transmural stimulation with a phasic spike contraction followed by a sustained contractile response. The sustained response was inhibited by phentolamine and guanethidine and thus apparently results from noradrenaline release from adrenergic nerves. Addition of 2–5 mM Cs+ greatly potentiated this secondary response without altering the sensitivity of the tissue to added (−)-noradrenaline. This potentiation was not due to Cs+ decreasing the neuronal uptake of noradrenaline, or by Cs+ altering prostaglandin synthesis. Addition of 2 mM Cs+ significantly increased the amount of (±)-[3H]metaraminol released from tissues in response to transmural stimulation (5 Hz). It is suggested that caesium potentiated responses of rabbit vas deferens to transmural stimulation by increasing the amount of transmitter released per nerve impulse, possibly as a result of prolongation of the action potential.

Some Pharmacological Effects of Prodolic Acid, a New Anti-inflammatory Compound, Indicative of Inhibition of Prostaglandin Synthesis

1975 ◽  
Vol 53 (1) ◽  
pp. 186-189 ◽  
Author(s):  
R. Greenberg
Keyword(s):  
Electrical Stimulation ◽  
Guinea Pig ◽  
Portal Vein ◽  
Vas Deferens ◽  
Prostaglandin Synthesis ◽  
Pharmacological Effects ◽  
Prostaglandin Biosynthesis ◽  
Inhibition Of Prostaglandin Synthesis ◽  
Anti Inflammatory ◽  
Rabbit Vas Deferens

Prodolic acid, a new non-steroidal anti-inflammatory compound, inhibited bradykinin-induced bronchoconstriction but did not affect histamine-induced bronchoconstriction in the guinea pig. Prodolic acid potentiated the responses of the isolated rabbit vas deferens and portal vein to electrical stimulation without altering the response to noradrenaline. The potentiating effects of prodolic acid on the vas deferens were reversible but the potentiating effects in the portal vein were frequency-dependent. It is concluded that these effects of prodolic acid are probably related to its ability to inhibit prostaglandin biosynthesis.

The potentiating effects of 4-aminopyridine on adrenergic transmission in the rabbit vas deferens

1976 ◽  
Vol 38 (1) ◽  
pp. 71-78 ◽  
Author(s):  
Anthony Johns ◽  
Donald S. Golko ◽  
Patricia A. Lauzon ◽  
David M. Paton
Keyword(s):  
Vas Deferens ◽  
Adrenergic Transmission ◽  
Rabbit Vas Deferens

Effect of neuronal uptake inhibitors on the adrenergic-neuron blockade produced by guanethidine in rabbit vas deferens

1977 ◽  
Vol 55 (3) ◽  
pp. 609-614 ◽  
Author(s):  
L. J. Huston ◽  
D. S. Golko ◽  
D. M. Paton
Keyword(s):  
Vas Deferens ◽  
Neuronal Uptake ◽  
Noradrenaline Uptake ◽  
Adrenergic Neuron ◽  
Serotonin Uptake Inhibitor ◽  
Uptake Inhibitors ◽  
Subsequent Exposure ◽  
Noradrenaline Uptake Inhibitors ◽  
Rabbit Vas Deferens ◽  
Sustained Responses

The effect of neuronal-uptake inhibitors on the guanethidine-induced inhibition of responses of rabbit vas deferens to transmural stimulation was investigated. The twitch and sustained reponses were inhibited by about 70% by 1.2 × 10−5 M guanethidine. Prior or subsequent exposure to the noradrenaline-uptake inhibitors, 3.3 × 10−5 M cocaine, 10−5 M nisoxetine, and 10−7 M desipramine prevented or reversed these effects of guanethidine. The depressant effects of guanethidine were not modified by the serotonin-uptake inhibitor, 10−6 M fluoxetine. The uptake of 5 × 10−8 M (−)-[3H]noradrenaline by rabbit vas deferens was significantly reduced by guanethidine, cocaine, nisoxetine, and desipramine, but not by fluoxetine. It was concluded that guanethidine inhibited both the twitch and sustained responses of the vas by producing adrenergic-neuron blockade and that these effects were dependent on continued transport into adrenergic neurons.

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