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Stretch-dependent slow force response in isolated rabbit myocardium is Na+ dependent
Dirk von Lewinski1, Burkhard Stumme, Lars S Maier
1Department of Cardiology and Pneumology, Georg-August-University, Robert-Koch-Str. 40, 37075, Göttingen, Germany.
Cardiovascular Research
|March 26, 2003
Summary
Stretch activates a slow force response in rabbit heart muscle, dependent on sodium and calcium but not pH or action potential duration. This inotropic effect involves Na+/H+-exchange and Na+/Ca2+-exchanger, not AT1 or ET(A) receptors.
Area of Science:
- Cardiovascular Physiology
- Cardiac Mechanics
- Cellular Electrophysiology
Background:
- Myocardial stretch triggers functional and trophic responses via signal transduction pathways.
- Understanding stretch-induced signaling is crucial for cardiac health and disease.
Purpose of the Study:
- To investigate stretch signal transduction mechanisms underlying immediate and slow force responses in rabbit myocardium.
- To elucidate the ionic and molecular players involved in stretch-induced inotropy.
Main Methods:
- Isolated rabbit ventricular muscles were subjected to rapid stretch.
- Functional force responses, sarcoplasmic reticulum Ca2+-load, intracellular pH, and action potential duration were measured.
- Pharmacological blockade and ionic manipulations assessed the roles of stretch-activated ion channels (SACs), AT1/ET(A) receptors, Na+/H+-exchange (NHE1), Na+/Ca2+-exchange (NCX), and Na+/K+-ATPase.
Main Results:
- Stretch induced an immediate force increase and a further, sustained Slow Force Response (SFR).
- SFR was significantly enhanced by increased sarcoplasmic reticulum Ca2+-load, independent of pH or action potential duration changes.
- SFR was dependent on Na+/H+-exchange and reverse mode Na+/Ca2+-exchange, and extracellular Na+ concentration, but not on SACs, AT1, or ET(A) receptors.
Conclusions:
- A delayed, Na+- and Ca2+-dependent Slow Force Response to stretch exists in rabbit myocardium.
- This inotropic response is independent of pH and action potential duration.
- The SFR is mediated by stretch-induced activation of Na+/H+-exchange and reverse mode Na+/Ca2+-exchange, independent of AT1 or ET(A) receptor activation.