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Titolo:
Endogenous tachykinins cause bradycardia by stimulating cholinergic neurons in the isolated guinea pig heart
Autore:
Chang, YZ; Hoover, DB; Hancock, JC;
Indirizzi:
E Tennessee State Univ, James H Quillen Coll Med, Dept Pharmacol, Johnson City, TN 37614 USA E Tennessee State Univ Johnson City TN USA 37614 hnson City, TN 37614 USA
Titolo Testata:
AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE PHYSIOLOGY
fascicolo: 6, volume: 278, anno: 2000,
pagine: R1483 - R1489
SICI:
0363-6119(200006)278:6<R1483:ETCBBS>2.0.ZU;2-P
Fonte:
ISI
Lingua:
ENG
Soggetto:
GENE-RELATED PEPTIDE; SUBSTANCE-P; IMMUNOREACTIVE NERVES; SENSORY NERVES; CO-EXISTENCE; CAPSAICIN; ANTAGONIST; RESINIFERATOXIN; NEUROPEPTIDE; BRADYKININ;
Keywords:
cardiac afferents; capsaicin; neurokinin A; calcitonin gene-related peptide; intrinsic cardiac ganglia;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
37
Recensione:
Indirizzi per estratti:
Indirizzo: Hoover, DB E Tennessee State Univ, James H Quillen Coll Med, Dept Pharmacol, Johnson City, TN 37614 USA E Tennessee State Univ Johnson City TN USA 37614 TN 37614 USA
Citazione:
Y.Z. Chang et al., "Endogenous tachykinins cause bradycardia by stimulating cholinergic neurons in the isolated guinea pig heart", AM J P-REG, 278(6), 2000, pp. R1483-R1489

Abstract

The purpose of this study was to determine if endogenous tachykinins can cause bradycardia in the isolated perfused guinea pig heart through stimulation of cholinergic neurons. Capsaicin was used to stimulate release of tachykinins and calcitonin gene-related peptide (CGRP) from cardiac afferents. A bolus injection of 100 nmol capsaicin increased heart rate by 26 +/- 7% from a baseline of 257 +/- 14 beats/min (n = 6, P < 0.01). This positive chronotropic response was converted to a minor bradycardic effect in hearts with 1 mu M CGRP-(8-37) present to block CGRP receptors. The negative chronotropic response to capsaicin was markedly potentiated in another group of hearts with the further addition of 0.5 mu M neostigmine to inhibit cholinesterases. In this group, capsaicin decreased heart rate by 30 +/- 10% from a baseline of 214 +/- 6 beats/min (n = 8, P < 0.05). This large bradycardic response to capsaicin was inhibited by 1) infusion of neurokinin A to desensitize tachykinin receptors or 2) treatment with 1 mu M atropine to block muscarinic receptors. The latter observations implicate tachykinins and acetylcholine, respectively, as mediators of the bradycardia. These findings support the hypothesis that endogenous tachykinins could mediate axon reflexesto stimulate cholinergic neurons of the intrinsic cardiac ganglia.

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Documento generato il 04/12/20 alle ore 18:32:54