| pubmed-article:3475521 | pubmed:abstractText | The responses to 9 X 10(-7) M vasoactive intestinal polypeptide (VIP) by isolated human basilar arteries of 30 individuals were studied to further elucidate the role the peptide might play in modifying cerebrovascular tone normally and in disease. In most experiments the artery was precontracted with prostaglandin F2 alpha (PGF2 alpha), either with 1 or 2 X 10(-6) M or with 10(-5) M PGF2 alpha. The course of action to VIP was observed for 15 min following its application to the contracted vessel. Some arteries failed to respond to VIP (13%), otherwise the arteries relaxed 44% when the contraction was induced by 10(-5) M PGF2 alpha and 67.6% after the lower concentrations of PGF2 alpha. There was no significant decrement in the vasorelaxant effect of VIP throughout the period of observation. A second and third application of VIP to the precontracted artery produced significantly less of an effect than the first, but no consistent progressive pattern of tachyphylaxis was evident. In additional experiments, indomethacin (10(-5) M) did not prevent the vasorelaxant effect of VIP, suggesting that prostanoid synthesis was not involved. Pretreatment of the artery with VIP did not prevent the contractions generated by 10, 30, 50 and 90 mM KCl while antithrombin III (1.2 X 10(-7) M) did, indicating fundamental differences between these two vasorelaxants. In conclusion, VIP will inhibit contraction of isolated human cerebral arteries for prolong periods and could be a significant factor regulating cerebral blood flow in humans. | lld:pubmed |
