AI Article Synopsis
- The neuropeptides PACAP and VIP interact with G protein-coupled receptors VPAC(1)-R and VPAC(2)-R to induce vasodilation in cerebral arteries.
- The study investigates the role of intramural neurons in this vasodilatory response using isolated rat basilar arteries and various signaling inhibitors.
- Findings indicate that N-type calcium channels and neuronal nitric oxide synthase play significant roles in mediating the relaxing effects of PACAP on vascular tone.
Article Abstract
The structurally related neuropeptides pituitary adenylate cyclase activating polypeptide (PACAP) and vasoactive intestinal polypeptide (VIP) are recognised by two G protein-coupled receptors, termed VPAC(1)-R and VPAC(2)-R, with equal affinity. PACAP and VIP have previously been shown to relax cerebral arteries in an endothelium-independent manner. The aim of the present study was to test if intramural neurons are involved in the mediation of PACAP/VIP-induced vasodilatory responses. Therefore, the vascular tone of isolated rat basilar arteries was measured by means of a myograph. The vasorelaxing effect of PACAP was assessed in arteries precontracted by serotonin in the absence or presence of different test compounds known to selectively inhibit certain signaling proteins. The vasorelaxant effect of PACAP could be significantly reduced by the inhibitor of neuronal N-type calcium channels omega-conotoxin GVIA (omega-CgTx), as well as by 3-bromo-7-nitroindazole (3Br-7-Ni), an inhibitor of the neuronal nitric oxide-synthase (nNOS). The localization of N-type calcium channels and VPAC-Rs within the rat basilar artery was investigated by confocal laser scanning microscopy using omega-CgTx- and VIP-analogs labelled with fluorescent dyes. These findings suggest that activation of intramural neurons may represent an important effector mechanism for mediation of the vasorelaxant PACAP-response.
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| http://dx.doi.org/10.1016/s0167-0115(02)00072-1 | DOI Listing |
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