AJP - Heart Watch the video to learn how APS reaches out to developing nations.
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
QUICK SEARCH:   [advanced]


     

Am J Physiol Heart Circ Physiol (September 16, 2004). doi:10.1152/ajpheart.00727.2004
This Article
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
288/1/H382    most recent
00727.2004v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Web of Science (10)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Xu, H.-L.
Right arrow Articles by Pelligrino, D. A
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Xu, H.-L.
Right arrow Articles by Pelligrino, D. A
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.




This article has been cited by other articles:


Home page
 StrokeHome page
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]

Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
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]

Home page
 Circ. Res.Home page
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]

Home page
 Exp PhysiolHome page
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]

Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
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]

Home page
 J. Appl. Physiol.Home page
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]

Home page
 Am. J. Physiol. Regul. Integr. Comp. Physiol.Home page
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]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
Visit Other APS Journals Online
Copyright © 1977 by the American Physiological Society.