AJP - Heart pressure measurements
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
QUICK SEARCH:   [advanced]


     

Am J Physiol Heart Circ Physiol (May 20, 2005). doi:10.1152/ajpheart.00276.2005
This Article
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
289/3/H1184    most recent
00276.2005v1
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 (6)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Armstead, W. M
Right arrow Articles by Hecker, J. G
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Armstead, W. M
Right arrow Articles by Hecker, J. G
Submitted on March 21, 2005
Accepted on May 11, 2005

Heat Shock Protein Modulation Of KATP And Kca Channel Cerebrovasodilation After Brain Injury

William M Armstead1* and James G Hecker2

1 Anesthesia, University of Pennsylvania, Philadelphia, PA, USA; Anesthesia, University of Pennsylvania, Philadelphia, PA, USA
2 Anesthesia, University of Pennsylvania, Philadelphia, PA, USA; Pharmacology, University of Pennsylvania, Philadelphia, PA, USA

* To whom correspondence should be addressed. E-mail: armsteaw{at}uphs.upenn.edu.

Fluid percussion brain injury (FPI) impairs pial artery dilation to activators of the ATP sensitive (KATP) and calcium activated (Kca) channel. This study investigated the role of heat shock protein (HSP) in the modulation of K channel induced pial artery dilation after FPI in newborn pigs equipped with a closed cranial window. Under non brain injury conditions, topical co-administration of exogenous HSP 27 (1 µg/ml) blunted dilation to cromakalim, calcitonin gene related peptide (CGRP), and NS 1619 (10-8, 10-6 M) (KATP and Kca agonists respectively). In contrast, co-administration of exogenous HSP 70 (1 µg/ml) potentiated dilation to cromakalim, CGRP, and NS 1619. FPI increased the CSF concentration of HSP 27 from 0.051 ± 0.012 to 0.113 ± 0.035 ng/ml but decreased the CSF concentration of HSP 70 from 50.42 ± 8.96 to 30.9 ± 9.9 ng/ml at 1 hour post insult. Pretreatment with topical exogenous HSP 70 (1 µg/ml) prior to FPI fully blocked injury induced impairment of cromakalim and CGRP dilation and partially blocked injury induced impairment of dilation to NS 1619. These data indicate that HSP 27 and HSP 70 contribute to modulation of K channel induced pial artery dilation. These data suggest that HSP 70 is an endogenous protectant whose actions may be unmasked and/or potentiated with exogenous administration prior to brain injury.




This article has been cited by other articles:


Home page
 Cardiovasc ResHome page
B. J.J.M. Brundel, L. Ke, A.-J. Dijkhuis, X. Qi, A. Shiroshita-Takeshita, S. Nattel, R. H. Henning, and H. H. Kampinga
Heat shock proteins as molecular targets for intervention in atrial fibrillation
Cardiovasc Res, June 1, 2008; 78(3): 422 - 428.
[Abstract] [Full Text] [PDF]

Home page
 Cardiovasc ResHome page
M. Sakabe, A. Shiroshita-Takeshita, A. Maguy, B. J.J.M. Brundel, A. Fujiki, H. Inoue, and S. Nattel
Effects of a heat shock protein inducer on the atrial fibrillation substrate caused by acute atrial ischaemia
Cardiovasc Res, April 1, 2008; 78(1): 63 - 70.
[Abstract] [Full Text] [PDF]

Home page
 J. Neurosci.Home page
G. A. B. Armstrong, K. L. Shoemaker, T. G. A. Money, and R. M. Robertson
Octopamine Mediates Thermal Preconditioning of the Locust Ventilatory Central Pattern Generator via a cAMP/Protein Kinase A Signaling Pathway.
J. Neurosci., November 22, 2006; 26(47): 12118 - 12126.
[Abstract] [Full Text] [PDF]


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