Interaction between ATP-sensitive K+ channels (KATP) and nitric oxide (NO) on pial arterioles in piglets

T. Louis, F. Bari, R. Errico, D. Busija

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Abstract

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.

Original languageEnglish
Pages (from-to)A585
JournalFASEB Journal
Volume10
Issue number3
Publication statusPublished - Dec 1 1996

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ASJC Scopus subject areas

  • Biotechnology
  • Biochemistry
  • Molecular Biology
  • Genetics

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