Bowditch effect
Encyclopedia
The Bowditch Effect is an autoregulation method by which myocardial contractility increases with an increase in heart rate. Also known as the Treppe phenomenon or Treppe effect.
One of the explanations is the inability of the Na+/K+-ATPase
to keep up with influx of sodium at higher heart rates. When a higher heart rate occurs, for example due to adrenergic stimulation, the L Type Calcium channel has increased activity. The 3Na+/Ca++ exchanger (which allows 3 Na to flow down its gradient in exhange for 1 Ca++ ion to flow out of the cell) works to decrease the levels of intracellular calcium. As the heart rate becomes more robust and the length of diastole decreases, the Na+/K+-ATPase which removes the Na+ brought into the cell by the Na/Ca exchanger does not keep up with the rate of Na influx. This leads to a less efficient Na/Ca exchange since the gradient is decreasing for sodium and therefore Ca++ builds up within the cell. This results in an accumulation of calcium in the myocardial cell via the sodium calcium exchanger. And leads to a greater state of inotropism, a mechanism which is also seen with cardiac glycosides.
Alternatively, another mechanism is that the Na+-Ca+ membrane exchanger, which operates continually, has less time to remove the Ca++ that arrives in the cell because of the decreased length of diastole with positive chronotropy. With an increased intracellular Ca++ concentration, there follows a positive inotropy.
One of the explanations is the inability of the Na+/K+-ATPase
Na+/K+-ATPase
Na+/K+-ATPase is an enzyme located in the plasma membrane in all animals.- Sodium-potassium pumps :Active transport is responsible for cells containing relatively high...
to keep up with influx of sodium at higher heart rates. When a higher heart rate occurs, for example due to adrenergic stimulation, the L Type Calcium channel has increased activity. The 3Na+/Ca++ exchanger (which allows 3 Na to flow down its gradient in exhange for 1 Ca++ ion to flow out of the cell) works to decrease the levels of intracellular calcium. As the heart rate becomes more robust and the length of diastole decreases, the Na+/K+-ATPase which removes the Na+ brought into the cell by the Na/Ca exchanger does not keep up with the rate of Na influx. This leads to a less efficient Na/Ca exchange since the gradient is decreasing for sodium and therefore Ca++ builds up within the cell. This results in an accumulation of calcium in the myocardial cell via the sodium calcium exchanger. And leads to a greater state of inotropism, a mechanism which is also seen with cardiac glycosides.
Alternatively, another mechanism is that the Na+-Ca+ membrane exchanger, which operates continually, has less time to remove the Ca++ that arrives in the cell because of the decreased length of diastole with positive chronotropy. With an increased intracellular Ca++ concentration, there follows a positive inotropy.