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Capsaicin-evoked bradycardia in anesthetized guinea pigs is mediated by endogenous tachykinins

Capsaicin-evoked bradycardia in anesthetized guinea pigs is mediated by endogenous tachykinins,10.1016/j.regpep.2007.12.001,Regulatory Peptides,John C

Capsaicin-evoked bradycardia in anesthetized guinea pigs is mediated by endogenous tachykinins   (Citations: 2)
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The present study was done to characterize the effects of endogenous tachykinins on heart rate in urethane-anesthetized guinea pigs. Intravenous injection of capsaicin (32 nmol/kg) was used to evoke release of tachykinins and calcitonin gene-related peptide (CGRP) from cardiac sensory nerve fibers. Such injections caused a brief decrease in heart rate (−37±7 beats/min, n=6) that was followed by a more prolonged increase (+44±10 beats/min). Blood pressure was lowered by −11±2 mmHg. Bilateral vagotomy did not affect the chronotropic or depressor responses to capsaicin, but atropine (1 µmol/kg) nearly abolished the bradycardic response (−8±3 beats/min, n=7). Combined blockade of NK2 and NK3 receptors, with SR48968 and SR14801 respectively, also caused a significant reduction of capsaicin-evoked bradycardia (−14±3 beats/min, n=4) but did not affect bradycardia evoked by vagal nerve stimulation. Blockade of CGRP receptors eliminated capsaicin-evoked tachycardia and prolonged the capsaicin-evoked bradycardia. These findings suggest that capsaicin-evoked bradycardia in the anesthetized guinea pig is mediated by tachykinins that stimulate cardiac cholinergic neurons. This effect appears to be truncated by the positive chronotropic action of CGRP that is also released from cardiac afferents by capsaicin.
Journal: Regulatory Peptides - REGUL PEPTIDES , vol. 147, no. 1, pp. 19-24, 2008
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    • ...Moreover, in anaesthetized guinea pigs it has been observed that capsaicin evokes a biphasic change of heart rate with a prominent bradycardia as an initial component [18] or a triphasic blood pressure response in anesthetized rat following intravenous administration of the TRPV1 agonist anandamide [19]...
    • ...On the other hand, the effect of NKA, which is co-stored with SP in capsaicin-sensitive nerves also causes bradycardia, but via both cholinergic and non-cholinergic nerves [18]...
    • ...rate previously reported following administration of a TRPV1 agonist [18,19] may be a result of pharmacokinetic properties...
    • ...It has been previously reported that the cardiovascular effects of SP [23,25], but not of NKA [18], could be prevented by atropine...

    Keld Fosgerauet al. Increased susceptibility to cardiovascular effects of dihydrocapcaicin...

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