Autonomic Neurotransmission

Hedqvist, Per

doi:10.1007/978-1-4615-8052-2_4

Cited by 55 publications

(23 citation statements)

References 105 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…There is discussion as to whether the release ofprostaglandins occurs from the nerve 568 PG-INDUCED INHIBITION OF ACh RELEASE (Stjarne, 1972;Greenberg, 1978;Petkov & Radomirov, 1980;Radomirov, Petkov & Venkova, 1981) or from the muscles in response to nerve stimulation (Gilmore, Vane & Wyllie, 1968;Hedqvist, 1973) in adrenergic neuro-effector transmission. The present results, with regard to the cholinergic neuro-effector transmission in the dog trachea, favour the view that the release of prostaglandins occurs mainly from nerves, since 5 X 10-6 M-atropine, which is a sufficient concentration to suppress the nerveinduced contraction of the smooth muscle cells, did not significantly reduce the amount of prostaglandins released in response to the field stimulations.…”

Section: Resultsmentioning

confidence: 99%

Prostaglandin‐induced inhibition of acetylcholine release from neuronal elements of dog tracheal tissue.

Inoue¹,

Ito²,

Takeda³

1984

The Journal of Physiology

View full text Add to dashboard Cite

In an attempt to elucidate the possible roles of endogenous prostaglandins on the neuro‐effector transmission in the dog trachea, effects of a prostaglandin antagonist (1‐acetyl‐2‐[8‐chloro‐10, 11‐ dihydrobenz (b.f) (1.4) oxazepine‐10‐carbonyl]hydrazine (SC‐19220] on the electrical and mechanical properties of smooth muscle cells and on neuro‐effector transmission in the smooth muscle layer were studied by means of micro‐electrode, double sucrose‐gap, and tension recording methods. The levels of prostaglandins in the perfusate from the dog tracheal tissue were also determined using radioimmunoassay. Excitatory junction potentials (e.j.p.s) and twitch tension evoked by electrical field stimulation with short pulse duration (50‐100 microseconds), which were abolished by tetrodotoxin (10(‐7) M) or atropine (5 X 10(‐6) M), showed gradual and continuous reduction in amplitude during superfusion with normal Krebs solution. Reduction in the amplitude of e.j.p.s occurred with no change in the membrane potential or membrane input resistance. SC‐19220 (3.1 X 10(‐5) M) did not modify the membrane potential, membrane input resistance or the sensitivity to acetylcholine of the smooth muscle cells. Yet, with application of SC‐19220 (3.1 X 10(‐6) M), gradual and continuous reductions in the amplitude of e.j.p.s and twitch contractions were no longer observed. With an increased concentration (3.1 X 10(‐5) M), e.j.p.s and twitch contractions with a constant amplitude were obtained after the initial increase in the amplitude. When the amplitude of twitch contractions was stabilized by treatment with indomethacin (10(‐5) M), low concentrations (10(‐12) to 10(‐10) M) of prostaglandin E2 (PGE2) or prostaglandin F2 alpha (10(‐8) to 10(‐6) M) markedly suppressed the amplitude of the twitch contractions. In some muscle preparations (ten out of twenty‐two preparations examined), SC‐19220 (3.1 X 10(‐6) to 3.1 X 10(‐5) M) produced a sustained contraction of the muscle, which was suppressed by atropine (5 X 10(‐6) M) or PGE2 (10(‐8) M). Following pre‐treatment of the tissue with atropine (5 X 10(‐6) M), SC‐19220 did not evoke contracture. In the resting condition, 10‐40 ng g‐1 wet wt. tissue min‐1 PGE or PGF was released into the perfusate from the tracheal muscle tissue of the control dog.(ABSTRACT TRUNCATED AT 400 WORDS)

show abstract

Section: Resultsmentioning

confidence: 99%

Prostaglandin‐induced inhibition of acetylcholine release from neuronal elements of dog tracheal tissue.

Inoue¹,

Ito²,

Takeda³

1984

The Journal of Physiology

View full text Add to dashboard Cite

show abstract

“…Animal studies indicate that the hypotensive action is largely due to an action on vascular smooth muscle resulting in dilatation of both resistance and capacitance vessels (Conway and Hatton, 1975). It has also been suggested that PG E2 may exert a negative feedback control over sympathetic neural transmission (Hedqvist, 1973) and this may have resulted in the diminished responses. It may be argued, however, that this latter action might impair the chance of successful ejaculation.…”

Section: Discussionmentioning

confidence: 99%

Severe hypertension in patients with high spinal cord lesions undergoing electro-ejaculation—Management with prostaglandin E2

Frankel

1980

Spinal Cord

View full text Add to dashboard Cite

“…In general, prostaglandins (PG's) ' appear to be ubiquitous and have been demonstrated to modulate a variety of tissue and hormone system effects (1 (2). Since the adrenergic nervous system has profound regulatory effects upon insulin secretion (3,4) In all of the studies to be described, intravenous glucose was injected as a 2-g pulse (4 ml of a 50% glucose solution) in less than 3 s. Unless otherwise indicated, all infusions other than the glucose injections were given through a catheter placed in the femoral vein opposite to the one used for sample collection.…”

Section: Introductionmentioning

confidence: 99%

Inhibition of In Vivo Insulin Secretion by Prostaglandin E1

Robertson¹,

Dj²,

Porte³

et al. 1974

J. Clin. Invest.

View full text Add to dashboard Cite

A B S T R A C T To determine the effect of prostaglandin E1 (PGE1) infusion upon in vivo insulin secretion, serum insulin responses after an intravenous glucose pulse (2 g) were measured before and during an intravenous infusion of PGE1 (10 Ag/min) in 11 anesthetized dogs. Circulating insulin decreased significantly during PGE1 infusion, and insulin responses after glucose during PGE1 infusion were significantly less than control responses. Three dogs received PGE1 infusions into the thoracic aorta to preclude pulmonic and hepatic degradation of PGE1 before its arrival at the pancreatic artery; inhibition of insulin secretion was again seen. Inhibition of insulin secretion could not be related to the degree of arterial hypotension induced by intravenous PGE1, and despite alpha adrenergic blockade with intravenous phentolamine, PGEi-induced inhibition of glucose-stimulated insulin responses persisted. Significant increments in systemically circulating PGE levels during intravenous PGE1 infusions were documented by radioimmunoassay. These studies demonstrate that systemic PGE1 infusion inhibits insulin secretion and that this effect could not be shown to be dependent upon alpha adrenergic activity.

show abstract

Autonomic Neurotransmission

Cited by 55 publications

References 105 publications

Prostaglandin‐induced inhibition of acetylcholine release from neuronal elements of dog tracheal tissue.

Prostaglandin‐induced inhibition of acetylcholine release from neuronal elements of dog tracheal tissue.

Severe hypertension in patients with high spinal cord lesions undergoing electro-ejaculation—Management with prostaglandin E2

Inhibition of In Vivo Insulin Secretion by Prostaglandin E1

Contact Info

Product

Resources

About