Kadota O, Ohta S, Kumon Y, Sakaki S, Matsuda S, Sakanaka M
Department of Neurological Surgery, Ehime University School of Medicine, Japan.
Neurosci Lett. 1995 Oct 20;199(2):99-102. doi: 10.1016/0304-3940(95)12040-b.
Using the cranial window method, we investigated the effect of basic fibroblast growth factor (bFGF) on the diameter of the rat basilar artery in vivo. bFGF (5-200 ng/ml) caused significant vasodilation in a dose-dependent manner with the maximal effect (119% of baseline diameter) at 200 ng/ml. Vasodilation was not observed when the basilar artery was treated with heat-inactivated bFGF or bFGF preincubated with bFGF-neutralizing monoclonal antibody. Moreover, bFGF-induced vasodilation was suppressed significantly by coadministration of the nitric oxide (NO) synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME). In contrast, NG-nitro-D-arginine methyl ester (D-NAME), which is the isomer of L-NAME, exerted no influence on bFGF-induced vasodilation. These findings suggest that the dilatation by bFGF of the rat basilar artery is mediated by NO, and that bFGF plays an important role in the regulation not only of the anterior circulation as previously described but also of the posterior circulation in the brain.
