Smith, Paula and McQueen, D S (2001) Anandamide induces cardiorespiratory reflexes via vasosensory nerves in the anaesthetized rat. British Journal of Pharmacology, 134 (3). pp. 655-663. ISSN 00071188

Abstract/Description

We tested the hypothesis that sensory nerves innervating blood vessels play a role in the local and systemic regulation of the cardiovascular and respiratory (CVR) systems. We measured CVR reflexes evoked by administration of anandamide (86 – 863 nmoles) and capsaicin (0.3 – 10 nmoles) into the hindlimb vasculature of anaesthetized rats.
Anandamide and capsaicin each caused a rapid dose-dependent reflex fall in blood pressure and an increase in ventilation when injected intra-arterially into the hindlimb.
Action of both agonists at the vanilloid receptor (VR1) on perivascular sensory nerves was investigated using capsazepine (1 mg kg-1 i.a.) a competitive VR1 antagonist, ruthenium red (1 mg kg-1 i.a.), a non-competitive antagonist at VR1, or a desensitizing dose of capsaicin (200 nmoles i.a.). The cannabinoid receptor antagonist SR141716 (1 mg kg-1 i.a.) was used to determine agonist activity at the CB1 receptor.
Capsazepine, ruthenium red, or acute VR1 desensitization by capsaicin-pretreatment, markedly attenuated the reflex CVR responses evoked by anandamide and capsaicin (P<0.05; paired Student's t-test). Blockade of CB1 had no significant effect on the responses to anandamide.
Local sectioning of the femoral and sciatic nerves attenuated CVR responses to anandamide and capsaicin (P<0.05). Vagotomy or carotid sinus sectioning had no significant effect on anandamide- or capsaicin-induced responses.
These data demonstrate that both the endogenous cannabinoid, anandamide, and the vanilloid, capsaicin, evoke CVR reflexes when injected intra-arterially into the rat hindlimb. These responses appear to be mediated reflexly via VR1 located on sensory nerve endings within the hindlimb vasculature.

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