Absence of effects of prostaglandins E1 and E2 on ganglionic transmission

Kayaalp, S. O.; McIsaac, Robert J.

doi:10.1016/0014-2999(68)90095-2

Cited by 17 publications

(5 citation statements)

References 14 publications

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“…the poorly understood, Ca-dependent events which are triggered by depolarizarion and result in secretion of transmitter from the nerves. sympathetic chain (Kayaalp and McIsaac 1968). The finding in the present study that PGEz did not change the amplitude of the action potentials in the bovine splenic nerves is in accordance with this observation.…”

Section: Discussionsupporting

confidence: 93%

Antagonism by Calcium of the Inhibitory Action of Prostaglandin E₂ on Sympathetic Neuro‐transmission in the Cat Spleen

Hedqvist

1970

Acta Physiologica Scandinavica

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HEDQVIST, P. i.!ntagonism by calcium of the inhibitory action of prostaglandin EZ on sympathetic neurotransmission in the cut spleen. Acta physiol. scand. 1970. 80. 269-275. Experiments werz carried out with the isolated, perfused cat spleen and bovine splenic nerve trunk to study the target for prostaglandin E2 induced inhibition of noradrenaline release from sympathetic nervzs. Increasing the calcium concentration in the medium perfusing the spleeen was found to increase the outflow of noradrenaline to nerve stimuiation and to antagonize the inhibitory action of prostaglandin Ez on this parameter. Prostaglandin E2 did not affect the noradrenaline releasing effect of tyramine. Atropine did not alter the inhibitory effect of prostaglandin Ez on noradrenaline release. Prostaglandin Ez did not change the amplitude of action potentials in bovine splenic nerves. There is thus no support for a blocking action on nerve conduction. It is concluded that prostaglandin E2 may prevent calcium from gaining access to those sites in sympathetic nerve terminals where it promotes secretion of noradrenaline. L

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Section: Discussionsupporting

confidence: 93%

Antagonism by Calcium of the Inhibitory Action of Prostaglandin E₂ on Sympathetic Neuro‐transmission in the Cat Spleen

Hedqvist

1970

Acta Physiologica Scandinavica

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“…PGE1 and PGE2 have been reported to have no effect on postganglionic action potentials elicited by preganglionic stimulation of the feline cervical sympa thetic chain (125). On the other hand, the observation that PGE1 is more prone to inhibit contractile responses to preganglionic than postganglionic nerve stimulation in the guinea pig vas deferens is consistent with PGE1 interfering with ganglionic transmission (126).…”

Section: Ganglionic Transmissionmentioning

confidence: 71%

Basic Mechanisms of Prostaglandin Action on Autonomic Neurotransmission

Hedqvist¹

1977

Annu. Rev. Pharmacol. Toxicol.

328

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“…Partly, this extremely high sensitivity of the hypogastric ganglion might be due to a favourable location of the nearly unprotected ganglion cells in the thin peritoneal cover at the base of the vas deferens. With regard to the negative reports concerning PG effects on ganglionic transmission (Kayaalp and McIsaas 1968) a true difference in comparison to other autonomic ganglia cannot, however, be excluded, since this peripheral sympathetic ganglion in the hypogastric nerve also shows other divergent pharmacological properties (Bentley 1968).…”

Section: Discussionmentioning

confidence: 99%

Endogenous Inhibition of the Mechanical Response of the Isolated Rat and Guinea‐Pig Vas Deferens to Pre‐ and Postganglionic Nerve Stimulation

Swedin

1971

Acta Physiologica Scandinavica

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Repeated periods with prolonged nerve stimulation (30 s) of the isolated vas deferens tended to depress especially the initial, rapid phase of subsequent contractions. The following findings led to the conclusion that the inhibition was induced by prostaglandin (PG)‐like material, released from the organ on nerve stimulation: 1. The inhibition was immediately abolished on washing of the organ. 2. It appeared faster in an organ bath of small volume than in one of a greater. 3. It was possible to transfer the substance from one bath to influence an organ in another. 4. The inhibitory agent, like exogenous PG, influenced both phases of contraction, the second, however, to a less extent. 5. The ganglionic transmission in the last part of the hypogastric nerve was found to be extremely sensitive to the inibitory substance as to exogenous PG (0.1–0.4 ng/ml). 6. In vitro inihibition of PG synthesis led to a partial or total abolishment of the endogenous inhibition. 7. Release upon nerve stimulation of PG‐like material, mainly PGE2, was established. It is suggested that this endogenous inhibiting process might play a modulating role in the nerve‐induced mechanical activity of this organ also under in vivo conditions.

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Absence of effects of prostaglandins E1 and E2 on ganglionic transmission

Cited by 17 publications

References 14 publications

Antagonism by Calcium of the Inhibitory Action of Prostaglandin E₂ on Sympathetic Neuro‐transmission in the Cat Spleen

Antagonism by Calcium of the Inhibitory Action of Prostaglandin E₂ on Sympathetic Neuro‐transmission in the Cat Spleen

Basic Mechanisms of Prostaglandin Action on Autonomic Neurotransmission

Endogenous Inhibition of the Mechanical Response of the Isolated Rat and Guinea‐Pig Vas Deferens to Pre‐ and Postganglionic Nerve Stimulation

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Absence of effects of prostaglandins E1 and E2 on ganglionic transmission

Cited by 17 publications

References 14 publications

Antagonism by Calcium of the Inhibitory Action of Prostaglandin E2 on Sympathetic Neuro‐transmission in the Cat Spleen

Antagonism by Calcium of the Inhibitory Action of Prostaglandin E2 on Sympathetic Neuro‐transmission in the Cat Spleen

Basic Mechanisms of Prostaglandin Action on Autonomic Neurotransmission

Endogenous Inhibition of the Mechanical Response of the Isolated Rat and Guinea‐Pig Vas Deferens to Pre‐ and Postganglionic Nerve Stimulation

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Product

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About

Antagonism by Calcium of the Inhibitory Action of Prostaglandin E₂ on Sympathetic Neuro‐transmission in the Cat Spleen

Antagonism by Calcium of the Inhibitory Action of Prostaglandin E₂ on Sympathetic Neuro‐transmission in the Cat Spleen