Journal of Applied Physiology Watch the video to see how APS reaches out to developing nations.
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

J Appl Physiol 96: 1425-1432, 2004. First published December 12, 2003; doi:10.1152/japplphysiol.01077.2003
8750-7587/04 $5.00
This Article
Right arrow Full Text Free
Right arrow Full Text (PDF) Free
Right arrow All Versions of this Article:
96/4/1425    most recent
01077.2003v1
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
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 (9)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Korzick, D. H.
Right arrow Articles by Bowles, D. K.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Korzick, D. H.
Right arrow Articles by Bowles, D. K.

Alterations in PKC signaling underlie enhanced myogenic tone in exercise-trained porcine coronary resistance arteries

D. H. Korzick,1,4 M. H. Laughlin,1,2,3 and D. K. Bowles1,3

Departments of 1Biomedical Sciences and 2Medical Pharmacology and Physiology and 3Dalton Cardiovascular Research Center, University of Missouri, Columbia, Missouri 65211; and 4Department of Kinesiology and Noll Physiological Research Center, The Pennsylvania State University, University Park, Pennsylvania 16802

Submitted 3 October 2003 ; accepted in final form 8 December 2003

The intracellular mechanisms underlying enhanced myogenic contraction (MC) in coronary resistance arteries (CRAs) from exercise-trained (EX) pigs have not been established. The purpose of this study was to test the hypothesis that exercise-induced alterations in protein kinase C (PKC) signaling underlie enhanced MC. Furthermore, we sought to determine whether modulation of intracellular Ca2+ signaling by PKC underlies enhanced MC in EX animals. Male Yucatan miniature swine were treadmill trained (n = 7) at ~75% of maximal O2 uptake for 16 wk (6 miles/h, 60 min) or remained sedentary (SED, n = 6). Diameter measurements in response to intraluminal pressure (60, 75, and 90 cmH2O) or 60 mM KCl were determined in single, cannulated CRAs (~100 µm ID) with and without the PKC inhibitor chelerythrine (CE, 1 µM). Confocal imaging of Ca2+ signaling [myogenic Ca2+ (Cam)] was also performed in CRAs of similar internal diameter after abluminal loading of the Ca2+ indicator dye fluo 4 (1 µM, 37°C, 30 min). We observed significantly greater MC in CRAs isolated from EX than from SED animals at 90 cmH2O, as well as greater reductions in MC after CE at all pressures studied. At intraluminal pressures of 75 and 90 cmH2O, CE produced greater decreases in Cam in CRAs from EX than from SED animals (64% vs. 25%, P < 0.05). Inhibition of KCl constriction and Cam by CE was also greater in EX animals (P < 0.05). Western blotting revealed significant increases in Ca2+-dependent PKC-{alpha} (~50%) but not Ca2+-independent PKC-{epsilon} levels in CRAs isolated from EX animals (P < 0.05). We also observed significant group differences in phosphorylated PKC-{alpha} levels. Finally, voltage-gated Ca2+ current (VGCC) was effectively blocked by CE, bisindolylmaleimide, and staurosporine in isolated smooth muscle cells from CRAs, providing evidence for a mechanistic link between VGCCs and PKC in our experimental paradigm. These results suggest that enhanced MC in CRAs from EX animals involves PKC-dependent modulation of intracellular Ca2+, including regulation of VGCCs.

protein kinase C; voltage-gated calcium channels


Address for reprint requests and other correspondence: D. K. Bowles, E102 Veterinary Medicine Bldg., Univ. of Missouri, Columbia, MO 65211 (E-mail: bowlesd{at}missouri.edu).




This article has been cited by other articles:


Home page
 Am. J. Physiol. Renal Physiol.Home page
S. Ghosh, M. Khazaei, F. Moien-Afshari, L. S. Ang, D. J. Granville, C. B. Verchere, S. R. Dunn, P. McCue, A. Mizisin, K. Sharma, et al.
Moderate exercise attenuates caspase-3 activity, oxidative stress, and inhibits progression of diabetic renal disease in db/db mice
Am J Physiol Renal Physiol, April 1, 2009; 296(4): F700 - F708.
[Abstract] [Full Text] [PDF]

Home page
 Physiol. Rev.Home page
D. J. Duncker and R. J. Bache
Regulation of Coronary Blood Flow During Exercise
Physiol Rev, July 1, 2008; 88(3): 1009 - 1086.
[Abstract] [Full Text] [PDF]

Home page
 Cardiovasc ResHome page
R. Schubert, D. Lidington, and S.-S. Bolz
The emerging role of Ca2+ sensitivity regulation in promoting myogenic vasoconstriction
Cardiovasc Res, January 1, 2008; 77(1): 8 - 18.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
C. A. Cobine, B. P. Callaghan, and K. D. Keef
Role of L-type calcium channels and PKC in active tone development in rabbit coronary artery
Am J Physiol Heart Circ Physiol, June 1, 2007; 292(6): H3079 - H3088.
[Abstract] [Full Text] [PDF]

Home page
 J. Physiol.Home page
G. C. Amberg, M. F. Navedo, M. Nieves-Cintron, J. D. Molkentin, and L. F. Santana
Calcium sparklets regulate local and global calcium in murine arterial smooth muscle
J. Physiol., February 15, 2007; 579(1): 187 - 201.
[Abstract] [Full Text] [PDF]

Home page
 Cardiovasc ResHome page
D. H. Korzick, J. M. Muller-Delp, P. Dougherty, C. L. Heaps, D. K. Bowles, and K. K. Krick
Exaggerated coronary vasoreactivity to endothelin-1 in aged rats: Role of protein kinase C
Cardiovasc Res, May 1, 2005; 66(2): 384 - 392.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online
Copyright © 2004 by the American Physiological Society.