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. Author manuscript; available in PMC: 2010 Aug 4.
Published in final edited form as: Brain Res. 2009 Jun 16;1283:50–57. doi: 10.1016/j.brainres.2009.06.021

Fig. 2.

Fig. 2

Characterization of VIP-induced pial arteriolar vasodilation. VIP elicited significant, dose-dependent, reproducible increases in pial arteriolar diameters, while artificial cerebrospinal fluid (aCSF) did not evoke vasodilation (A). The non-selective cyclooxygenase (COX) inhibitor indomethacin abolished the pial arteriolar dilation in response to 10–8 M VIP, whereas it left the vasodilation to higher concentrations (10–7–10–6 M) of VIP essentially intact (B). The pial arteriolar response to VIP was differentially affected by selective COX inhibitors; the COX-1 inhibitor SC-560 abolished the arteriolar responses to 10–8 M VIP (C), whereas the COX-2 inhibitor NS-398 was ineffective (D). (Data are mean±SEM, n=6–8, *p<0.05: significantly higher than vasodilation to all smaller VIP concentrations, †p<0.05: significantly less than the corresponding value before treatment.)