Abstract
The effects of capsaicin and selective neuropeptide antagonists on pial artery diameter were measured using an on-line image analyser in anaesthetised cats, in order to monitor the effects of mediators released in response to activation of trigeminal nerves. Perivascular injection of CGRP (10(-8) M) and the neurokinin-1 (NK1) receptor agonist substance P methyl ester, SPOMe (10(-6) M) produced an increase in pial artery diameter. The vasodilatory action of these agonists was significantly and selectively inhibited using the CGRP receptor antagonist, CGRP8-37 (10(-6) M), and the NK1 receptor antagonist, CP99994 (10(-6) M) respectively. Capsaicin (10(-8)-10(-5) M) produced a biphasic response upon perivascular injection that was concentration dependent. At 10(-6) M capsaicin an initial transient vasoconstriction was observed followed by a longer-lasting vasodilatation. The vasodilator component was significantly reduced by CGRP8-37 (10(-6) M) or CP99994 (10(-6) M). These results show that chemical (capsaicin) activation of trigeminal nerves leads to vasodilatation of feline arteries in situ. This vasodilatation is mediated via the activation of CGRP and NK1 receptors probably via the efferent release of CGRP and a substance P-like peptide.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
