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Am J Physiol Heart Circ Physiol (August 8, 2002). doi:10.1152/ajpheart.00391.2002
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Articles in PresS, published online ahead of print August 8, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00391.2002
Submitted on May 6, 2002
Accepted on August 3, 2002

Interaction between increased SERCA2a activity and ß-adrenoceptor function in adult rabbit myocytes

Babar Chaudhri1, Federica del Monte2, Roger Hajjar2, and Sian E Harding1*

1 Faculty of Medicine, Imperial College of Science, Technology and Medicine, London, United Kingdom
2 Cardiovascular Research Centre, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA

* To whom correspondence should be addressed. E-mail: sian.harding{at}ic.ac.uk.

SERCA2a overexpression or phospholamban depletion have been shown to have beneficial effects on contractility in heart failure. However, the high sympathetic tone during development of failure may interact with increases in SERCA2a activity in potentially deleterious ways. We have used adenoviral vectors to overexpress SERCA2a or partially down-regulate phospholamban in adult rabbit ventricular myocytes in culture, and studied the responses of these cells to ß-adrenoceptor stimulation. SERCA2a overexpression or phospholamban depletion had quantitatively similar effects on basal contraction amplitude and in accelerating relaxation. Increasing SERCA2a activity by either strategy had little effect on the increase in contraction amplitude or incidence of arrhythmias with increasing isoproterenol. Maximum acceleration of relaxation by ß-adrenoceptor stimulation was similar to that produced by SERCA2a overexpression. Isoproterenol treatment of SERCA2a-overexpressing or phospholamban-deficient myocytes produced a modest further decrease in relaxation time, with final values similar in both groups. We find no evidence for calcium overload induced by SERCA2a overexpression alone or in combination with catecholamines.




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