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Articles in PresS, published online ahead of print November 23, 2001
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00523.2001
Submitted on June 15, 2001
Accepted on November 21, 2001
1 Physiology and Pharmacology, Wake Forest University School of Medicine, Winston-Salem, NC, USA; Physiology, University of Szeged, Szeged, Hungary
2 Physiology and Pharmacology, Wake Forest University School of Medicine, Winston-Salem, NC, USA
3 Physiology, University of Szeged, Szeged, Hungary
* To whom correspondence should be addressed. E-mail: domoki{at}phys.szote.u-szeged.hu.
N-methyl-D-aspartate (NMDA) elicits pial arteriolar dilation that has been associated with neuronal nitric oxide (NO) production. However, endothelial factors or glial P-450 epoxygenase products may play a role. We tested if NMDA-induced pial vasodilation (1) primarily involves NO diffusion from the parenchyma to the surface arterioles, (2) involves intact endothelial function, and (3) involves a miconazole-sensitive component. Arteriolar diameters were determined using closed cranial window/intravital microscopy in anesthetized piglets. NMDA (10-100µM) elicited virtually identical dose-dependent dilations in paired arterioles (r=0.94, n=15). However, NMDA but not bradykinin (BK) induced dilations of arteriolar sections over large veins was reduced by 31±1% (mean±S.E.M, p<0.05, n=4) compared to adjacent sections on the cortical surface. Also, 100µM NMDA increased cerebrospinal fluid levels of NO metabolites from 3.7±1.0 to 5.3±1.2 µM (p<0.05, n=6). Endothelial stunning by intracarotid injection of phorbol 12,13-dibutyrate did not affect NMDA-induced vasodilation, but attenuated vascular responses to hypercapnia and BK by ~70% (n=7,7,7). Finally, miconazole (n=6, 20µM) pretreatment and coapplication with NMDA did not alter vascular responses to NMDA. In conclusion, NMDA appears to dilate pial arterioles exclusively through release and diffusion of NO from neurons to the pial surface in piglets.
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