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Angiotensin II and phorbol esters depress cardiac performance and decrease diastolic and systolic [Ca2+]i in isolated
J Wikman-Coffelt1, S T Wu, W W Parmley
1Department of Medicine, University of California San Francisco 94143.
American Heart Journal
|September 1, 1991
Summary
Angiotensin II and PMA reduce heart function by decreasing intracellular calcium transients. This impacts developed pressure, oxygen consumption, and coronary flow in rat hearts.
Area of Science:
- Cardiovascular Physiology
- Cellular Signaling
Background:
- Angiotensin II and phorbol 12-myristate 13-acetate (PMA) are known modulators of cardiac function.
- Intracellular calcium handling is critical for myocardial contractility.
Purpose of the Study:
- To investigate the effects of Angiotensin II and PMA on cardiac function and intracellular calcium in isolated perfused rat hearts.
- To elucidate the mechanisms underlying the observed functional changes.
Main Methods:
- Isolated perfused rat heart model.
- Measurement of developed pressure, oxygen consumption, and coronary flow.
- Assessment of intracellular calcium ([Ca2+]i) levels and transients.
Main Results:
- Both Angiotensin II and PMA significantly depressed developed pressure, oxygen consumption, and coronary flow.
- These agents decreased diastolic and systolic intracellular calcium ([Ca2+]i) and [Ca2+]i transients.
- A moderate decrease in phosphocreatine/creatine (PCr/Cr) ratio was observed, without changes in cAMP levels.
- Hearts treated with Angiotensin II and PMA showed reduced sensitivity to extracellular calcium.
Conclusions:
- The reduction in cardiac function by Angiotensin II and PMA is attributed to decreased systolic [Ca2+]i and impaired [Ca2+]i transients.
- Lowered intracellular calcium levels likely fall below the threshold for effective cross-bridge interaction, leading to depressed cardiac performance.