INTERACTION BETWEEN ATP-SENSITIVE K-OXIDE ON PIAL ARTERIOLES IN PIGLETS( CHANNELS AND NITRIC)

The interaction between ATP-sensitive K+ channels (K-ATP) and nitric o xide (NO) was studied in pial arterioles of piglets. We examined the e ffects of N-omega-nitro-L-arginine methyl ester (L-NAME), a general in hibitor of nitric oxide synthase (NOS), and 7-nitroindazole (7-NI), a selective inhibitor of neuronal NOS, on aprikalim-induced cerebral vas odilation. Topically applied, aprikalim, a selective activator of K-AT P, dilated arterioles by 11 +/- 7% at 10(-8) M and 17 +/- 6% at 10(-6) M. After L-NAME treatment (15 mg/kg, i.v.). the response was reduced (4 +/- 4% and 12 +/- 7%, respectively; n = 8, p < 0.05). Administratio n of 7-NI (50 mg/kg, i.p.) did not change pial arteriolar responsivene ss to aprikalim. However, both L-NAME and 7-NI reduced the vasodilator responses to 10(-4) M N-methyl-D-aspartate (NMDA) (by 73% and by 36%, respectively). Furthermore, 7-NI treatment abolished the glutamate-in duced dilatation of pial arterioles. Administration of L-NAME reduced the NOS activity in the cerebral cortex by 88%, whereas the reduction after the 7-NI treatment was 44%. Pretreatment anti coadministration o f 10(-5) M glibenclaminde, a specific inhibitor of K-ATP or L-NAME adm inistration, did not change the dilatory response to sodium nitropruss ide. We conclude that NO may be involved in aprikalim-induced dilation of pial arterioles.