Modulation of N-methyl-D-aspartate (NMDA)-induced cerebral arteriolar dilation by hypoxia in piglets

F. Bari, T. M. Louis, D. W. Busija

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Abstract

Cerebral arteriolar responses to NMDA are suppressed by oxygen radicals produced during reoxygenation following short-term arterial hypoxia (Stroke 27:1634, 1996). However, vascular responses to NMDA during hypoxia have not been examined. We tested the hypotheses that bioactive substances released during hypoxia or hypoxia alone would reduce NMDA-induced arteriolar dilation. Pial arteriolar diameter was determined in anesthetized piglets via intravital microscopy. Baseline arteriolar diameters were ∼ 100 μm. Topical application of NMDA at concentrations of 10-5, 5×10-5 and 10-4 mol/l resulted in dose-dependent vasodilation (9±2%, 19±2% and 30±2% above baseline, respectively, n=20). NMDA-induced vasodilation was not modified after application of sodium nitroprusside (SNP, 10-5 mol/l) or when SNP (10-7 mol/l) was coapplied with NMDA (n=6). Coapplication of adenosine (10-6 mol/l) attenuated NMDA responses (31±5% vs 20±3% dilation, n=7). Administration of theophylline (20 mg/kg, iv.) had no effect on NMDA-dependent vasodilation but blocked dilation to hypoxia (inhalation of 7.5% O2). NMDA responses were completely abolished during hypoxia (28±2% vs 2±1%, respectively to 10-4 mol/l, n=7). However, SNP still dilated pial arterioles. We conclude, that hypoxia has direct and indirect effect on NMDA induced vasodilation.

Original languageEnglish
Pages (from-to)A22
JournalFASEB Journal
Volume11
Issue number3
Publication statusPublished - Dec 1 1997

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ASJC Scopus subject areas

  • Biotechnology
  • Biochemistry
  • Molecular Biology
  • Genetics

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