Hypertension, Vol 8, 583-591, Copyright © 1986 by American Heart Association
RV Sharma, CA Butters and RC Bhalla
Spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto (WKY)
rats were used to investigate the adaptive biochemical changes in the
myocardium in response to chronic afterload. Ouabain-inhibited
Na+,K+-adenosine triphosphatase (ATPase) activity was decreased by 40% in
myocardium of SHR compared with that from WKY, which may lead to increased
intracellular Ca2+ through Na+-Ca2+ exchange. Similarly, alpha 1-adrenergic
receptor density, estimated by [3H]prazosin binding, was decreased by 42%
in myocardial membranes of SHR, while the affinity for the agonist and the
antagonist was not altered. In contrast, the number of Ca2+ channels
estimated by [3H]nitrendipine binding was increased by 45% in myocardial
membranes of SHR, while the affinity was comparable between SHR and WKY.
These differences between WKY and SHR in the membrane properties were not
due to differential contamination of plasma membranes because the
activities of other putative plasma membrane marker enzymes were comparable
between WKY and SHR. There were no differences between WKY and SHR in the
myosin ATPase activity estimated using myofibrils, actomyosin, and myosin.
These results suggest that specific alterations have occurred in the plasma
membrane properties of myocardium of SHR that result in altered
intracellular Ca2+ metabolism. These alterations may have an important
bearing on excitation-contraction coupling in myocardium of SHR.
ARTICLES
Alterations in the plasma membrane properties of the myocardium of spontaneously hypertensive rats
This article has been cited by other articles:
![]() |
R. A. Brown, A. O. Savage, and T. C. Lloyd Influence of Age on the Inotropic Response to Acute Ethanol Exposure in Spontaneously Hypertensive Rats Hypertension, November 1, 1996; 28(5): 872 - 879. [Abstract] [Full Text] |
||||
|
Hypertension Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 1986 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |