Local cardiac effects of substance P: roles of acetylcholine and noradrenaline

Research output: Contribution to journalArticle

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Abstract

The local cardiac actions of substance P were examined in isolated perfused hearts and atria of the guinea‐pig. In both hearts and right atria, substance P caused negative inotropic and chronotropic effects. Atropine (10−6 m) or depletion of acetylcholine, by electrical stimulation and hemicholinium‐3 perfusion, significantly attenuated the negative inotropic and chronotropic effects of substance P. α‐ and β‐adrenoceptor blockade by nadolol and phentolamine (10−6 m each) did not prevent the negative inotropic and chronotropic effects of substance P. This indicates that cholinergic neurones, but not adrenergic neurones, partially mediate the effects of substance P. There was no significant difference in the effects of substance P observed between groups with acetylcholine depletion and with cholinoceptor blockade. This suggests that substance P elicits its effects mainly through release of acetylcholine. These results indicate that substance P has negative inotropic and chronotropic effects in guinea‐pig hearts and right atria mediated partly by release of acetylcholine. Substance P also appears to have direct effects on cardiac tissue. 1995 British Pharmacological Society

Original languageEnglish (US)
Pages (from-to)283-288
Number of pages6
JournalBritish Journal of Pharmacology
Volume114
Issue number2
DOIs
StatePublished - Jan 1995

Fingerprint

Substance P
Acetylcholine
Norepinephrine
Heart Atria
Nadolol
Adrenergic Neurons
Cholinergic Neurons
Phentolamine
Cholinergic Receptors
Atropine
Adrenergic Receptors
Electric Stimulation
Perfusion

Keywords

  • Substance P
  • acetylcholine
  • heart
  • local cardiac actions
  • noradrenaline
  • right atria

ASJC Scopus subject areas

  • Pharmacology

Cite this

Local cardiac effects of substance P : roles of acetylcholine and noradrenaline. / Chiao, Hsi; Caldwell, Robert W.

In: British Journal of Pharmacology, Vol. 114, No. 2, 01.1995, p. 283-288.

Research output: Contribution to journalArticle

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