HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 90/5/755    most recent expphysiol.2005.030908v1 Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Burniston, J. G Articles by Goldspink, D. F Search for Related Content PubMed PubMed Citation Articles by Burniston, J. G Articles by Goldspink, D. F Related Collections Muscle

¹ Research Institute for Sport & Exercise Sciences, Liverpool John Moores University, Webster Street, Liverpool L3 2ET, UK ² Academic Unit of Molecular Vascular Medicine, University of Leeds, Leeds General Infirmary, Leeds LS2 9JT, UK

Our previous work has established that angiotensin II is cardiotoxic. Here we sought to investigate whether skeletal muscle is similarly susceptible to damage. Male Wistar rats were either given a single subcutaneous injection of angiotensin II (range 1 µg kg^–1 to 10 mg kg^–1) or only the vehicle and killed 7 h later, or implanted with preconditioned osmotic pumps dispensing 1 mg kg^–1 day^–1 angiotensin II and killed 9 or 18 h later. Apoptotic (caspase 3 positive) myocytes were counted on cryosections of the heart, soleus, tibialis anterior and diaphragm muscle. Single injections of 100 µg kg^–1 to 10 mg kg^–1 angiotensin II induced significant (P < 0.05) myocyte apoptosis (per 10⁴ viable myocytes) in the heart and this was heterogeneously distributed, peaking (5.7 ± 0.6; P < 0.05) at a point 6 mm from the apex, i.e. approximately three-quarters of the way towards the base. The slow-twitch soleus muscle was also damaged significantly (peak = 2.6 ± 0.4; P < 0.05), while only the administration of 1 mg kg^–1 induced significant (P < 0.05) apoptosis in the fast-twitch tibialis anterior muscle (peak = 1.2 ± 0.3). Infusion of 1 mg kg^–1 day^–1 angiotensin II induced more myocyte apoptosis than a single bolus administration of the same dose, and in general there was a higher incidence of apoptosis in muscles harvested after 18 than after 9 h. Infusion of 1 mg kg^–1 day^–1 angiotensin II over 18 h induced significant (P < 0.05) myocyte apoptosis in the heart (3.3 ± 0.4), soleus (3.9 ± 1), tibialis anterior (5.9 ± 0.4) and diaphragm (19.8 ± 5.6) muscle. Depending on the muscle type, angiotensin II induces myocyte apoptosis in skeletal muscle to a similar or greater extent as in cardiac muscle, supporting the hypothesis that angiotensin II is generally toxic to all striated muscles.

(Received 14 May 2005; accepted after revision 28 June 2005; first published online 29 June 2005)
Corresponding author J. G. Burniston, Research Institute for Sports and Exercise Sciences, Liverpool John Moores University, Webster Street, Liverpool L3 2ET, UK. Email: j.burniston{at}livjm.ac.uk

This article has been cited by other articles:

				P. Li, R. E. Waters, S. I. Redfern, M. Zhang, L. Mao, B. H. Annex, and Z. Yan Oxidative Phenotype Protects Myofibers from Pathological Insults Induced by Chronic Heart Failure in Mice Am. J. Pathol., February 1, 2007; 170(2): 599 - 608. [Abstract] [Full Text] [PDF]

				J. G. Burniston, L.-B. Tan, and D. F. Goldspink Relative myotoxic and haemodynamic effects of the {beta}-agonists fenoterol and clenbuterol measured in conscious unrestrained rats Exp Physiol, November 1, 2006; 91(6): 1041 - 1049. [Abstract] [Full Text] [PDF]

				J. Quadrilatero and J. W. E. Rush Increased DNA fragmentation and altered apoptotic protein levels in skeletal muscle of spontaneously hypertensive rats J Appl Physiol, October 1, 2006; 101(4): 1149 - 1161. [Abstract] [Full Text] [PDF]