CA2-INDUCED CONTRACTION IN CANINE BASILAR ARTERY( HANDLING MECHANISMSUNDERLYING NEUROPEPTIDE Y)

The effects of neuropeptide Y on isometric tension simultaneously meas ured with cytosolic Ca2+ concentration ([Ca2+](cyt)) and Ca2+ sensitiv ity of contractile elements were studied in isolated canine basilar ar teries. Neuropeptide Y (1-100 nM) increased [Ca2+](cyt) and tension in a concentration-dependent and parallel manner, whereas 9,11-dideoxy-1 1 alpha,9 alpha-epoxymethano prostaglandin F-2 alpha (U46619) (10-100 nM), a thromboxane A(2) mimetic, produced a large contraction with a s mall increase in [Ca2+](cyt). Ca2+ channel antagonists such as d-cis-d iltiazem (10 mM) abolished both [Ca2+](cyt) and tension augmented by n europeptide Y. In Ca2+-free solution containing 0.2 mM EGTA, neuropept ide Y did not change [Ca2+](cyt) and tension, whereas U46619 transient ly increased both of them. Furthermore, neuropeptide Y apparently did not affect the Ca2+ sensitivity when assessed in the artery permeabili zed with Staphylococcus aureus alpha-toxin, whereas U46619 augmented i t. These findings suggest that neuropeptide Y-induced contraction in t he canine basilar artery is produced mainly by Ca2+ influx through L-t ype Ca2+ channels.