Previous investigations have indicated that
calcitonin gene-related peptide (CGRP), a principal transmitter in
capsaicin-sensitive sensory nerves, could alleviate cardiac
anaphylaxis injury.
Rutaecarpine relaxes vascular smooth by stimulation of CGRP release via activation of
vanilloid receptor subtype 1 (VR1). In the present study, we examined the role of
capsaicin-sensitive sensory nerves in anaphylactic vessels and the effect of
rutaecarpine on
antigen-challenged constriction in the guinea pig isolated thoracic aorta. The aortas were challenged with 0.01 mg/ml
bovine serum albumin, and the tension of aorta rings was continuously monitored. The amount of CGRP released from thoracic aortas was determined in the absence or presence of
rutaecarpine.
Antigen challenge caused a
vasoconstrictor response concomitantly with an increase in the release of CGRP from the isolated thoracic aorta, and the
vasoconstrictor responses were potentiated by
CGRP8-37 (10 microM) or
capsaicin (1 microM). Pretreatment with
diphenhydramine (1 microM) markedly decreased
antigen-challenged vasoconstriction. Acute application of
capsaicin (0.03 or 0.1 microM) significantly inhibited
vasoconstrictor responses. Pretreatment with
rutaecarpine (10 or 30 microM) significantly increased CGRP release concomitantly with decrease in
antigen-challenged vasoconstriction, which was abolished by
CGRP8-37 (10 microM) or
capsazepine (10 microM). The present results suggest that an increase in the release of CGRP during vascular
anaphylaxis may be a beneficial compensatory response, and that
rutaecarpine inhibits
antigen-challenged vasoconstriction, which is related to stimulation of endogenous CGRP release via activation of VR1.