AJP - Heart Calcium Transients and Cell-Sarcomere
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Heart Circ Physiol 280: H668-H673, 2001;
0363-6135/01 $5.00
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
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 ISI 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 ISI Web of Science (7)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Abe, K.
Right arrow Articles by Ibii, N.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Abe, K.
Right arrow Articles by Ibii, N.
Vol. 280, Issue 2, H668-H673, February 2001

Involvement of iNOS in postischemic heart dysfunction of stroke-prone spontaneously hypertensive rats

Kohji Abe, Miwa Tokumura, Tetsuji Ito, Takashi Murai, Akira Takashima, and Nobuhiro Ibii

Department of Drug Safety Evaluation, Developmental Research Laboratories, Shionogi & Co., Ltd., Toyonaka, Osaka 561-0825, Japan

We investigated the possible contribution of inducible nitric oxide synthase (iNOS) to postischemic heart dysfunction and injuries in stroke-prone spontaneously hypertensive rats (SHRSP). SHRSP, 13-14 wk of age, had significantly higher systolic blood pressure and greater heart weight than age-matched Wistar-Kyoto rats (WKY). Permanent occlusion of the left anterior descending coronary artery (LAD) caused significant and long-lasting increases in the activity and mRNA expression of myocardial iNOS in SHRSP compared with WKY. However, there was no significant difference in the LAD occlusion-induced expression of interleukin-1beta mRNA between SHRSP and WKY. Hemodynamic deterioration and myocardial fibrosis were also observed in SHRSP at 4 wk after LAD occlusion. Continuous administration of 2-amino-5,6-dihydro-6-methyl-4H-1,2-thiazin (AMT) completely blocked the LAD occlusion-induced increase in the myocardial iNOS activity of SHRSP. Moreover, postischemic heart dysfunction and injuries were also significantly ameliorated by 2-amino-5,6-dihydro-6-methyl-4H-1,2-thiazin (AMT). These results suggest that the increased activity of myocardial iNOS plays a pivotal role in the development of postischemic cardiac dysfunction and injuries in SHRSP with the hypertensive and hypertrophic heart.

cardiac hypertrophy; left anterior descending coronary artery occlusion; 2-amino-5,6-dihydro-6-methyl-4H-1,2-thiazin


This article has been cited by other articles:


Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
G. R. Norton, D. G. A. Veliotes, O. Osadchii, A. J. Woodiwiss, and D. P. Thomas
Susceptibility to systolic dysfunction in the myocardium from chronically infarcted spontaneously hypertensive rats
Am J Physiol Heart Circ Physiol, January 1, 2008; 294(1): H372 - H378.
[Abstract] [Full Text] [PDF]

Home page
 Exp PhysiolHome page
T. Itoh, M. Haruna, and K. Abe
Heart/Cardiac Muscle: Differential regulation of the nitric oxide-cGMP pathway exacerbates postischaemic heart injury in stroke-prone hypertensive rats
Exp Physiol, January 1, 2007; 92(1): 147 - 159.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
Y.-H. Liu, O. A. Carretero, O. H. Cingolani, T.-D. Liao, Y. Sun, J. Xu, L. Y. Li, P. J. Pagano, J. J. Yang, and X.-P. Yang
Role of inducible nitric oxide synthase in cardiac function and remodeling in mice with heart failure due to myocardial infarction
Am J Physiol Heart Circ Physiol, December 1, 2005; 289(6): H2616 - H2623.
[Abstract] [Full Text] [PDF]

Home page
 HypertensionHome page
Y. Sun, O. A. Carretero, J. Xu, N.-E. Rhaleb, F. Wang, C. Lin, J. J. Yang, P. J. Pagano, and X.-P. Yang
Lack of Inducible NO Synthase Reduces Oxidative Stress and Enhances Cardiac Response to Isoproterenol in Mice With Deoxycorticosterone Acetate-Salt Hypertension
Hypertension, December 1, 2005; 46(6): 1355 - 1361.
[Abstract] [Full Text] [PDF]

Home page
 J. Appl. Physiol.Home page
L. Zhang, C. G. Looney, W.-N. Qi, L.-E. Chen, A. V. Seaber, J. S. Stamler, and J. R. Urbaniak
Reperfusion injury is reduced in skeletal muscle by inhibition of inducible nitric oxide synthase
J Appl Physiol, April 1, 2003; 94(4): 1473 - 1478.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online