Inhibitory histamine H3-receptors on cholinergic nerves in human airways

Masakazu Ichinose; Peter J. Barnes

doi:10.1016/0014-2999(89)90212-4

Inhibitory histamine H₃-receptors on cholinergic nerves in human airways

Masakazu Ichinose, Peter J. Barnes

Research output: Contribution to journal › Article › peer-review

103 Citations (Scopus)

Abstract

The histamine H₃-agonist, (R)-α-methylhistamine (α-MeHA) caused a dose-dependent inhibition of cholinergic contractile responses to electrical field stimulation in human bronchi without affecting the basal tone. α-MeHA, but, did not alter the response to acetylcholine. Blockade of H₁- and H₂-receptors, or α- and β-adrenoceptors failed to prevent the inhibitory effect of α-MeHA, whereas the specific H₃-antagonist, thioperamide, was effective. Our results indicate that H₃-receptors modulate cholinergic neurotransmission in human airways.

Original language	English
Pages (from-to)	383-386
Number of pages	4
Journal	European Journal of Pharmacology
Volume	163
Issue number	2-3
DOIs	https://doi.org/10.1016/0014-2999(89)90212-4
Publication status	Published - 1989 Apr 25
Externally published	Yes

Keywords

(Human)
(R)-α-Methylhistamine
Bronchi
Electrical field stimulation
Histamine H-receptor agonists

ASJC Scopus subject areas

Pharmacology

Access to Document

10.1016/0014-2999(89)90212-4

Fingerprint Dive into the research topics of 'Inhibitory histamine H<sub>3</sub>-receptors on cholinergic nerves in human airways'. Together they form a unique fingerprint.

Cite this

@article{8fbf12a6aa2f45119efca8b47b50519c,

title = "Inhibitory histamine H3-receptors on cholinergic nerves in human airways",

abstract = "The histamine H3-agonist, (R)-α-methylhistamine (α-MeHA) caused a dose-dependent inhibition of cholinergic contractile responses to electrical field stimulation in human bronchi without affecting the basal tone. α-MeHA, but, did not alter the response to acetylcholine. Blockade of H1- and H2-receptors, or α- and β-adrenoceptors failed to prevent the inhibitory effect of α-MeHA, whereas the specific H3-antagonist, thioperamide, was effective. Our results indicate that H3-receptors modulate cholinergic neurotransmission in human airways.",

keywords = "(Human), (R)-α-Methylhistamine, Bronchi, Electrical field stimulation, Histamine H-receptor agonists",

author = "Masakazu Ichinose and Barnes, {Peter J.}",

year = "1989",

month = apr,

day = "25",

doi = "10.1016/0014-2999(89)90212-4",

language = "English",

volume = "163",

pages = "383--386",

journal = "European Journal of Pharmacology",

issn = "0014-2999",

publisher = "Elsevier",

number = "2-3",

}

TY - JOUR

T1 - Inhibitory histamine H3-receptors on cholinergic nerves in human airways

AU - Ichinose, Masakazu

AU - Barnes, Peter J.

PY - 1989/4/25

Y1 - 1989/4/25

N2 - The histamine H3-agonist, (R)-α-methylhistamine (α-MeHA) caused a dose-dependent inhibition of cholinergic contractile responses to electrical field stimulation in human bronchi without affecting the basal tone. α-MeHA, but, did not alter the response to acetylcholine. Blockade of H1- and H2-receptors, or α- and β-adrenoceptors failed to prevent the inhibitory effect of α-MeHA, whereas the specific H3-antagonist, thioperamide, was effective. Our results indicate that H3-receptors modulate cholinergic neurotransmission in human airways.

AB - The histamine H3-agonist, (R)-α-methylhistamine (α-MeHA) caused a dose-dependent inhibition of cholinergic contractile responses to electrical field stimulation in human bronchi without affecting the basal tone. α-MeHA, but, did not alter the response to acetylcholine. Blockade of H1- and H2-receptors, or α- and β-adrenoceptors failed to prevent the inhibitory effect of α-MeHA, whereas the specific H3-antagonist, thioperamide, was effective. Our results indicate that H3-receptors modulate cholinergic neurotransmission in human airways.

KW - (Human)

KW - (R)-α-Methylhistamine

KW - Bronchi

KW - Electrical field stimulation

KW - Histamine H-receptor agonists

UR - http://www.scopus.com/inward/record.url?scp=0024477374&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0024477374&partnerID=8YFLogxK

U2 - 10.1016/0014-2999(89)90212-4

DO - 10.1016/0014-2999(89)90212-4

M3 - Article

C2 - 2721579

AN - SCOPUS:0024477374

VL - 163

SP - 383

EP - 386

JO - European Journal of Pharmacology

JF - European Journal of Pharmacology

SN - 0014-2999

IS - 2-3

ER -