&NA;The influence of subarachnoid hemorrhage (SAH) on vasodilatation induced by vasoactive intestinal polypeptide (VIP) was investigated in rabbit basilar arteries. VIP‐induced relaxation was measured in ring sections of the basilar arteries precontracted by 10‐5M serotonin using an isometric tension recording method. The cyclic adenosine monophosphate (cAMP) content was measured using radioimmunoassay as an indicator of the intracellular mechanism in the arterial smooth muscle cells. VIP (10‐11‐10‐6M) evoked dose‐dependent relaxation of the basilar arteries. The relaxation achieved with 10‐6M VIP was 85 ± 4% (n = 7) of the initial contractile tone in control arteries and 47 ± 5% (n = 8) in the arteries evaluated 2 days after SAH, suggesting that VIP‐induced relaxation was suppressed significantly after SAH (P< 0.01). The cAMP content was significantly higher in the basilar arteries 2 days after SAH (425 ± 48 pmol/g of tissue, n = 7) than in the control basilar arteries (194 ± 57 pmol/g of tissue, n = 7). In normal arteries, the cAMP content was increased to a significant degree by VIP (10‐6M) (325 ± 60% of control cAMP content, n = 5), whereas the increase was less in the arteries evaluated 2 days after SAH (112 ± 16% of control cAMP content, n = 5). These results suggest that SAH has an influence on cAMP metabolism in the arteries and that SAH impairs the postsynaptic mechanism of VIP‐induced dilatation of the arteries. (Neurosurgery24:731‐735, 1989)