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Am J Physiol Heart Circ Physiol (September 16, 2004). doi:10.1152/ajpheart.00727.2004
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Submitted on July 20, 2004
Accepted on September 14, 2004

The role of the glia limitans in ADP-induced pial arteriolar relaxation in intact and ovariectomized female rats

Hao-Liang Xu1, Shuhua Ye1, Verna L Baughman1, Douglas L Feinstein1, and Dale A Pelligrino1*

1 Neuroanesthesia Research, Univ. of Illinois at Chicago, Chicago, IL, USA

* To whom correspondence should be addressed. E-mail: dpell{at}uic.edu.

We examined whether the glia limitans (GL) influences pial arteriolar relaxation elicited in vivo by the purinergic (P2Y1 receptor) agonist, ADP, in female rats, and whether that influence is altered in ovariectomized (OVX) females. A validated model for GL injury was used-topical application of the gliotoxin, L-{alpha}-aminoadipic acid (L-{alpha}AAA), 24h prior to study. In both intact and OVX females, L-{alpha}AAA had no effect on responses to the NO donor, SNAP, but ADP-induced pial arteriolar dilations were significantly reduced (by 33-90%), compared to vehicle-treated controls. Upon addition of L-NNA to L-{alpha}AAA-treated rats, the ADP response was virtually lost in intact females, but no further reductions were observed in the OVX rats. On the other hand, in L-{alpha}AAA-treated OVX females, when the gap junction blocker, Gap 27, was subsequently added to the suffusate, ADP reactivity fell to very low levels. In vehicle-treated control rats, L-NNA and Gap 27 reduced ADP reactivity by ~50% in intact and OVX females, respectively. An earlier study indicated that the endothelium was a key site of influence for L-NNA (intact) and Gap 27 (OVX). Thus, present and previous results imply that the ADP response in pial arterioles represents the additive actions of an endothelial and a GL component. That supposition was confirmed, in the present study, by the finding that combining endothelial and GL injury produced an essentially complete loss of ADP reactivity in both intact and OVX females. Finally, topical application of the selective P2Y1 antagonist, MRS-2179, was associated with a nearly complete suppression of the ADP response in both intact and OVX females. These results suggest that: 1) ADP-induced pial arteriolar dilation involves additive contributions from P2Y1 receptors present both in vascular endothelium and the GL; 2) the influence of the GL component is not altered by ovariectomy; and 3) the gap junction-dependent component of the ADP response in OVX females is unlikely to include the GL and probably resides in the vessels themselves.




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