Actions of Tachykinins Within the Heart and Their Relevance to Cardiovascular Disease

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Substance P and neurokinin A are tachykinins that are co-localized with calcitonin gene-related peptide (CGRP) in a unique subpopulation of cardiac afferent nerve fibers. These neurons are activated by nociceptive stimuli and exhibit both sensory and motor functions that are mediated by the tachykinins and/or CGRP. Sensory signals (e.g., cardiac pain) are transmitted by peptides released at central processes of these neurons, whereas motor functions are produced by the same peptides released from peripheral nerve processes. This review summarizes our current understanding of intracardiac actions of the tachykinins. The major targets for the tachykinins within the heart are the intrinsic cardiac ganglia and coronary arteries. Intrinsic cardiac ganglia contain cholinergic neurons that innervate the heart and coronary vasculature. Tachykinins can stimulate NK<SUB>3</SUB> receptors on these neurons to increase their excitability and evoke spontaneous firing of action potentials. This action provides a mechanism whereby tachykinins can indirectly influence cardiac function and coronary tone. Tachykinins also have direct effects on coronary arteries to decrease or increase tone. Stimulation of NK<SUB>1</SUB> receptors on the endothelium causes vasodilation mediated by nitric oxide. This effect is normally dominant, but NK<SUB>2</SUB> receptor-mediated vasoconstriction can also occur and is augmented when NK<SUB>1</SUB> receptors are blocked. It is proposed that these ganglion stimulant and vascular actions are manifest by endogenous tachykinins during myocardial ischemia.


  • The Japanese Journal of Pharmacology

    The Japanese Journal of Pharmacology 84(4), 367-373, 2000-12-01

    The Japanese Pharmacological Society

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Cited by:  1


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