HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 288/1/H382    most recent 00727.2004v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (10) Citing Articles via Google Scholar Google Scholar Articles by Xu, H.-L. Articles by Pelligrino, D. A. Search for Related Content PubMed PubMed Citation Articles by Xu, H.-L. Articles by Pelligrino, D. A.

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

Neuroanesthesia Research, University of Illinois at Chicago, Chicago, Illinois

Submitted 20 July 2004 ; accepted in final form 14 September 2004

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--aminoadipic acid (L-AAA), 24 h before the study. In both intact and Ovx females, L-AAA had no effect on responses to the NO donor, S-nitroso-N-acetyl penicillamine, but ADP-induced pial arteriolar dilations were significantly reduced (by 33–90%), compared with vehicle-treated controls. When N^G-nitro-L-arginine (L-NNA) was administered to L-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-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 in both 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.

endothelium-derived hyperpolarizing factor; gap junction; nitric oxide; purinergic receptor

This article has been cited by other articles:

				A. Kanu and C. W. Leffler Roles of Glia Limitans Astrocytes and Carbon Monoxide in Adenosine Diphosphate-Induced Pial Arteriolar Dilation in Newborn Pigs Stroke, March 1, 2009; 40(3): 930 - 935. [Abstract] [Full Text] [PDF]

				H.-L. Xu, L. Mao, S. Ye, C. Paisansathan, F. Vetri, and D. A. Pelligrino Astrocytes are a key conduit for upstream signaling of vasodilation during cerebral cortical neuronal activation in vivo Am J Physiol Heart Circ Physiol, February 1, 2008; 294(2): H622 - H632. [Abstract] [Full Text] [PDF]

				A. Li, Q. Xi, E. S. Umstot, L. Bellner, M. L. Schwartzman, J. H. Jaggar, and C. W. Leffler Astrocyte-Derived CO Is a Diffusible Messenger That Mediates Glutamate-Induced Cerebral Arteriolar Dilation by Activating Smooth Muscle Cell KCa Channels Circ. Res., February 1, 2008; 102(2): 234 - 241. [Abstract] [Full Text] [PDF]

				H.-L. Xu and D. A. Pelligrino ATP release and hydrolysis contribute to rat pial arteriolar dilatation elicited by neuronal activation Exp Physiol, July 1, 2007; 92(4): 647 - 651. [Abstract] [Full Text] [PDF]

				C. W. Leffler, H. Parfenova, A. L. Fedinec, S. Basuroy, and D. Tcheranova Contributions of astrocytes and CO to pial arteriolar dilation to glutamate in newborn pigs Am J Physiol Heart Circ Physiol, December 1, 2006; 291(6): H2897 - H2904. [Abstract] [Full Text] [PDF]

				R. C. Koehler, D. Gebremedhin, and D. R. Harder Role of astrocytes in cerebrovascular regulation J Appl Physiol, January 1, 2006; 100(1): 307 - 317. [Abstract] [Full Text] [PDF]

				T. Kawaguchi, S. W. Brusilow, R. J. Traystman, and R. C. Koehler Glutamine-dependent inhibition of pial arteriolar dilation to acetylcholine with and without hyperammonemia in the rat Am J Physiol Regulatory Integrative Comp Physiol, June 1, 2005; 288(6): R1612 - R1619. [Abstract] [Full Text] [PDF]