Relaxation of sheep cerebral arteries by vasoactive intestinal polypeptide and neurogenic stimulation: inhibition by l‐NG‐monomethyl arginine in endothelium‐denuded vessels

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Abstract
Perivascular nerves of the sheep middle cerebral artery show immunoreactivity for both vasoactive intestinal polypeptide (VIP) and calcitonin gene‐related peptide (CGRP). Rings of endothelium‐denuded sheep middle cerebral artery precontracted with 5‐hydroxytryptamine were relaxed by CGRP (maximum relaxation = 87.8 ± 8.1%, pD2 = 7.81 ± 0.12, n = 12) and by VIP (maximum relaxation = 55.1 ± 4.1%, pD2 = 7.65 ± 0.04, n = 18). Rings of endothelium‐denuded cat middle cerebral artery precontracted with U46619 were also relaxed by vasoactive intestinal polypeptide (maximum relaxation = 53.1 ± 6.1%, pD2 = 7.82 ± 0.11, n = 6). Haemolysate (1 μl ml−1) inhibited VIP‐induced relaxation in endothelium‐denuded sheep and cat middle cerebral artery (n = 6) but had no effect on the CGRP‐induced relaxation of the sheep middle cerebral artery (n = 6). The relaxant response to VIP in endothelium‐denuded sheep middle cerebral artery was inhibited by methylene blue (10 μm) and augmented by either M&B 22948 (10 μm) or superoxide dismutase (150 units ml−1). Indomethacin (1 μm) had no effect. The addition of l‐NG‐monomethyl arginine (100 μm) inhibited both neurogenic and VIP‐induced relaxation of endothelium‐denuded sheep MCA by 56 ± 6% and 60 ± 6% (n = 5) respectively. The CGRP‐induced relaxation was unaffected. It is concluded that neurally mediated vasodilatation in the sheep middle cerebral artery is mediated largely by VIP through a direct action on smooth muscle through a cyclic‐GMP‐mediated mechanism that appears to involve synthesis of nitric oxide from l‐arginine. Vasodilatation by CGRP, which is also contained in perivascular nerves, does not utilize this pathway.

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