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Articles in PresS, published online ahead of print February 7, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00911.2001
Submitted on October 18, 2001
Accepted on January 31, 2002
1 Physiology, University of Tennessee, Memphis, TN, USA
* To whom correspondence should be addressed. E-mail: cleffler{at}physiol.utmem.edu.
The current study addressed the hypothesis that glutamate dilates pial arterioles of newborn pigs through the production of CO. Anesthetized newborn pigs were equipped with cranial windows in order to measure pial arteriolar responses to stimuli. Heme oxygenase inhibitors added topically inhibited dilation to glutamate and to specific glutamate receptor agonists. Initial dilation to glutamate (10-5M) was 22% from baseline without an inhibitor and decreased to 9% with the heme oxygenase inhibitor, chromium mesoporphyrin (CrMP). Inhibition of dilation upon heme oxygenase inhibition was similar when specific glutamate receptor agonists were employed. RS-AMPA dilated to 24% from the baseline without an inhibitor, and the dilation was decreased to 1% with tin protoporphyrin (SnPP). ATPA (kainate receptors) dilated 18% from baseline without an inhibitor, but only 2% when tin mesoporphyrin was applied. ACPD (NMDA) dilated pial arterioles 33% from baseline in control, but only to 2% in the presence of SnPP. Neither copper mesoporphyrin, which does not inhibit heme oxygenase, nor light inactivated CrMP effected the dilations. These data suggest that dilation of newborn pig pial arterioles to glutamate and specific glutamate-receptor agonists involves production of CO.
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