| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Neuroanesthesia Research Laboratory, University of Illinois at Chicago, Chicago, Illinois 60607
We examined pial
arteriolar reactivity to a partially endothelial nitric oxide synthase
(eNOS)-dependent vasodilator ADP as a function of chronic estrogen
status. The eNOS-dependent portion of the ADP response was ascertained
by comparing ADP-induced pial arteriolar dilations before and after
suffusion of a NOS inhibitor, N
-nitro-L-arginine
(L-NNA; 1 mM) in intact, ovariectomized (Ovx), and
17
-estradiol (E2)-treated Ovx females. We also examined
whether ovariectomy altered the participation of other factors in the ADP response. Those factors were the following: 1) the
prostanoid indomethacin (Indo); 2) the
Ca2+-dependent K+ (KCa) channel,
iberiotoxin (IbTX); 3) the ATP-regulated K+
(KATP) channel glibenclamide (Glib); 4) the
KCa-regulating epoxygenase pathway miconazole (Mic); and
5) the adenosine receptor 8-sulfophenyltheophylline (8-SPT).
In intact females, the eNOS-dependent (L-NNA sensitive) portion of the ADP response represented ~50% of the total. The ADP
response was retained in the Ovx rats but L-NNA sensitivity disappeared. On E2 replacement, the initial pattern was
restored. ADP reactivity was unaffected by Indo, Glib, Mic, and 8-SPT.
IbTX was associated with 50-80% reductions in the response to ADP
in the intact group that was nonadditive with L-NNA, and
60-100% reductions in the Ovx group. The present findings suggest
that estrogen influences the mechanisms responsible for ADP-induced vasodilation. The continued sensitivity to IbTX in Ovx rats, despite the loss of a NO contribution, is suggestive of a conversion to a
hyperpolarizing factor dependency in the absence of E2.
ATP-sensitive K+ channel; Ca2+-dependent K+ channel; endothelium-derived hyperpolarizing factor; miconazole; nitric oxide
This article has been cited by other articles:
|
|
 |
|
  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]
|
|
|
|
 |
|
 D. N. Krause, S. P. Duckles, and D. A. Pelligrino Influence of sex steroid hormones on cerebrovascular function J Appl Physiol, October 1, 2006; 101(4): 1252 - 1261. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. Andresen, N. I. Shafi, and R. M. Bryan Jr. Endothelial influences on cerebrovascular tone J Appl Physiol, January 1, 2006; 100(1): 318 - 327. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H.-L. Xu, S. Ye, V. L. Baughman, D. L. Feinstein, and D. A. Pelligrino The role of the glia limitans in ADP-induced pial arteriolar relaxation in intact and ovariectomized female rats Am J Physiol Heart Circ Physiol, January 1, 2005; 288(1): H382 - H388. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
F. M. Faraci, C. Lynch, and K. G. Lamping Responses of cerebral arterioles to ADP: eNOS-dependent and eNOS-independent mechanisms Am J Physiol Heart Circ Physiol, December 1, 2004; 287(6): H2871 - H2876. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
H. L. Xu, R. A. Santizo, V. L. Baughman, and D. A. Pelligrino Nascent EDHF-mediated cerebral vasodilation in ovariectomized rats is not induced by eNOS dysfunction Am J Physiol Heart Circ Physiol, November 1, 2003; 285(5): H2045 - H2053. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
H. L. Xu, R. A. Santizo, V. L. Baughman, and D. A. Pelligrino ADP-induced pial arteriolar dilation in ovariectomized rats involves gap junctional communication Am J Physiol Heart Circ Physiol, September 1, 2002; 283(3): H1082 - H1091. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 E. M. Golding, S. P. Marrelli, J. You, and R. M. Bryan Jr Endothelium-Derived Hyperpolarizing Factor in the Brain: A New Regulator of Cerebral Blood Flow? Stroke, March 1, 2002; 33(3): 661 - 663. [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |
