We examined the contribution of NO to arteriolar dilation caused by activation of KATP in anesthetized, newborn piglets Baseline arteriolar diameters were ∼ 100μm. Aprikalim, a selective activator of KATP, dilated arterioles by 12±1% at 10-8 M and 18±1% at 10-6 M (n=7, P<0.05). Administration of glibenclamide (10-5M), a selective inhibitor of KATP, blocked arteriolar dilation to aprikalim but not to sodium nitroprusside (10-5 and 10-5 M, n=7). Following L-NAME treatment (15 mg/kg, iv), vasodilator responses to aprikalim were reduced (n=7). However, administration of 7-nitroindazole (7-NI), a specific inhibitor of brain NOS, (50 mg/kg, ip) did not change the arteriolar responsiveness to aprikalim (n=5). In contrast, both L-NAME and 7-NI reduced or abolished the vasodilator responses to 10-4 M NMDA or glutamate. Using the citrulline conversion assay, we found that administration of L-NAME reduced the NOS activity in the cerebral cortex by 88%, whereas the reduction after the 7-NI treatment was 56% (P<0.05). We conclude that NO may be involved in aprikalim-induced dilation of pial arterioles, and that the source of NO might be from endothelium.
|Publication status||Published - Dec 1 1996|
ASJC Scopus subject areas
- Molecular Biology