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

Inoue, Toshiro; Ito, Yushi; Takeda, Kazuo

doi:10.1113/jphysiol.1984.sp015173

Cited by 46 publications

(39 citation statements)

References 20 publications

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“…, and was confirmed by other research groups using the same tissue (Walters, Obyrne, Fabbri, Graf, Holtzman & Nadel, 1984). With application of indomethacin, twitch contractions and e.j.p.s with a constant amplitude were obtained after the initial increase in the amplitude (Inoue et al 1984;Walters et al 1984). This observation suggests that endogenous prostaglandins are responsible for the time-and stimulation-dependent reduction in the size of twitch contractions and e.j.p.s.…”

Section: Discussionsupporting

confidence: 72%

“…The decline of the twitch contraction elicited by stimulation was overcome by application of indomethacin (10-5 M) ( Fig. l B and C), as was also noted in the dog trachea a, Inoue, Ito & Takeda, 1984.…”

Section: Methodssupporting

confidence: 68%

“…1A, the size of the twitch contractions, elicited by nerve stimulation every 3 min in the presence of propranolol (5 x 10-7 M, see below) gradually decreased. However, the reduction in the amplitude was relatively small, compared to that observed in the dog trachea (Inoue, Ito & Takeda, 1984), and the relative amplitude never decreased to less than 50 % of the initial value during prolonged perfusion (1-2 h). Fig.…”

Section: Methodsmentioning

confidence: 53%

“…This observation suggests that endogenous prostaglandins are responsible for the time-and stimulation-dependent reduction in the size of twitch contractions and e.j.p.s. Supporting this view, the amount of prostaglandin E or F series released into the perfusate increased, time-dependently (Walter et al 1984) or stimulation-dependently (Inoue et al 1984), in parallel to the reduction in the size of twitch contractions and e.j.p.s. Furthermore, a prostaglandin antagonist (SC-19220) prevented the fade phenomena of twitch contractions and e.j.p.s.…”

Section: Discussionmentioning

confidence: 96%

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Characteristics of neuro‐effector transmission in the smooth muscle layer of dog bronchiole and modifications by autacoids.

Inoue¹,

Ito²

1986

The Journal of Physiology

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Electrical and mechanical properties of smooth muscle cells and of neuro‐effector transmission in the smooth muscle layer of the dog bronchiole (about 1 mm in diameter) were studied with double‐sucrose‐gap, micro‐electrode or tension recording methods. Electrical field stimulation of short duration (50 microseconds) applied to the whole tissue excited the intrinsic nerves, and evoked excitatory junction potentials (e.j.p.s) followed by a twitch‐like tension; these were abolished by tetrodotoxin (10(‐7) M) or by atropine (10(‐6) M). 5‐Hydroxytryptamine (10(‐5) M) produced a tonic contracture of the bronchiole, and electrical field stimulation applied during the tonic contracture produced an initial phasic contraction and a subsequent relaxation. Atropine (10(‐6) M) and propranolol (10(‐6) M) selectively abolished the phasic contraction and relaxation, respectively, indicating that dog bronchiolar muscles are innervated by excitatory cholinergic and inhibitory adrenergic nerve fibres. E.j.p.s and twitch contractions evoked by electrical field stimulation at 3 min intervals showed a gradual reduction in amplitude during superfusion with normal Krebs solution, and this reduction was overcome by pre‐treatment with indomethacin (10(‐5) M). The mean value of the resting membrane potential of the bronchiole smooth muscle cells was ‐70.2 +/‐ 2.2 mV (+/‐ S.D., n = 150), and an action potential was superimposed on e.j.p.s in 50% of the muscle cells examined when the amplitude of e.j.p.s exceeded 35 mV. During repetitive field stimulation at 0.1‐0.2 Hz, the amplitude of the e.j.p.s gradually increased (facilitation); this phenomenon was markedly enhanced by indomethacin (10(‐5) M) and was depressed by exogenously applied prostaglandins in low concentrations (10(‐11)‐10(‐8) M). Histamine (5 X 10(‐8)‐5 X 10(‐7) M) enhanced the amplitude of e.j.p.s and twitch contraction evoked by field stimulation, and this effect was antagonized by mepyramine (10(‐7) M). Histamine (10(‐7) M) enhanced the amplitude of the ACh‐induced contraction when a relatively low concentration (10(‐7) M) of ACh was applied, but not when concentrations of 10(‐6) M‐ or 10(‐5) M‐ACh were applied. Histamine had no effects on the facilitation of e.j.p. Bronchiolar smooth muscle cells therefore showed larger resting potentials and a greater tendency to fire action potentials than trachealis muscle, and prostaglandins and histamine are involved in inhibitory and accelerative mechanisms related to excitatory neuro‐effector transmission, respectively.

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Section: Discussionsupporting

confidence: 72%

Section: Methodssupporting

confidence: 68%

Section: Methodsmentioning

confidence: 53%

Section: Discussionmentioning

confidence: 96%

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Characteristics of neuro‐effector transmission in the smooth muscle layer of dog bronchiole and modifications by autacoids.

Inoue¹,

Ito²

1986

The Journal of Physiology

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“…PACAP suppressed the eNANC-mediated contraction without affecting SP sensitivity at 10 -9 and 10 -8 M, which suggested that PACAP inhibited SP release from eNANC. By contrast, PACAP inhibited SP sensitivity at 10 -7 M. Although we did not employ direct measurements of ACh or SP in the present study, the release of ACh or SP was inferred from a comparison of the contractile responses to EFS and to exogenous ACh or SP as for the previous reports [25][26][27][28], and it was concluded that PACAP is likely to suppress the release of ACh or SP from nerve termini.…”

Section: Discussionmentioning

confidence: 68%

Pituitary adenylate cyclase activating peptide regulates neurally mediated airway responses

Shigyo¹,

Aizawa²,

Inoue³

et al. 1998

Eur Respir J

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Pituitary adenylate cyclase activating peptide (PACAP) is a vasoactive intestinal peptide (VIP)-like peptide that has been purified from the ovine hypothalami [1]. PACAP has the same potency as VIP in relaxing airway and vascular smooth muscle [2][3][4][5]. Recently, it has been demonstrated that PACAP induced bronchodilatation in animals treated with histamine or allergen [6]. However, the pathophysiological roles of PACAP in mammalian airways have not been fully elucidated. The structural and functional homology between PACAP and VIP makes it likely that PACAP may participate in the modulation of airway responses in a similar manner to VIP.VIP immunoreactivity is localized to the vagus nerve in the smooth muscle of mammalian airways [7][8][9]. It has been reported that VIP inhibits cholinergic neuroeffector transmission by suppressing acetylcholine (ACh) release from vagal nerve termini [10]. PACAP may have the same effects on cholinergic nerves. It has also been reported that VIP suppresses the smooth muscle contraction evoked by substance P (SP) [11]. SP belongs to the tachykinin family and is released from bronchial C-fibres, causing smooth muscle contraction and plasma extravasation [12].Increased plasma extravasation and smooth muscle contraction mediated by the vagus nerve may contribute to the airway hyperresponsiveness and inflammation observed in asthma. However, it is not known whether SP and PACAP interact.For these reasons, in the present study, we examined the roles of PACAP involved in airway smooth muscle response and plasma extravasation induced by cholinergic and excitatory nonadrenergic noncholinergic (eNANC) nerves in guinea-pigs. Methods Immunohistochemical examinationLungs were dissected out from three guinea-pigs after sacrifice. The specimens were immersed for 12 h in an ice-cold fixative solution composed of 2% formaldehyde buffered to pH 7.2 with 0.1 M phosphate buffer and 0.2% picric acid. They were then rinsed in a Tyrode solution containing 10% sucrose for 48 h, frozen on dry ice, and sectioned by a cryostat at a thickness of 10 µm. Then, they were immersed in sucrose-enriched Tyrode solution for 24-48 h, briefly rinsed in 0.1 M phosphate buffer (pH 7.4), and stretched on chrome-alum subbed glass slides as whole mounts. Cryostat sections and whole mounts were processed for immunohistochemical demonstration of PACAP using an avidin-biotin complex method. The PACAP antiserum (Yanaihara Institute Inc., Shizuoka, Japan) was raised in a rabbit against human PACAP 27 or PACAP 38 and used at a dilution of 1:12,000. The sections were exposed to the peptide antiserum for 4 h at room temperature. The antigen-antibody reaction was demonstrated by application of biotin-labelled anti-rabbit immunoglobulin G (IgG) Smooth muscle contraction evoked by electrical field stimulation (EFS) or exogenously applied acetylcholine (ACh) or substance P (SP) was measured before and after PACAP in vitro. The effect of PACAP on airway plasma extravasation was also measured in vivo.In trachea, PACAP (10 -9 -10 -...

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Membrane Phospholipid Metabolism and Transmitters

Berridge¹

1987

Receptor-Receptor Interactions

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

Cited by 46 publications

References 20 publications

Characteristics of neuro‐effector transmission in the smooth muscle layer of dog bronchiole and modifications by autacoids.

Characteristics of neuro‐effector transmission in the smooth muscle layer of dog bronchiole and modifications by autacoids.

Pituitary adenylate cyclase activating peptide regulates neurally mediated airway responses

Membrane Phospholipid Metabolism and Transmitters

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