cardiac myocytes การใช้

• Carvedilol reversibly binds to beta adrenergic receptors on cardiac myocytes.
• Normally, Ccna2 is silenced postnatally in mammalian cardiac myocytes.
• GLAST is also expressed in a number of other tissues including cardiac myocytes.
• Meanwhile, advances in the methods of obtaining cardiac myocytes in vitro occurred.
• In cardiac myocytes this forms a scalloped surface.
• CsA has been shown to decrease cardiac hypertrophy by affecting cardiac myocytes in many ways.
• The electrical depolarizations that trigger cardiac myocytes to contract arise spontaneously within the myocyte itself.
• Cardiac rhabdomyomas are hamartomas composed of altered cardiac myocytes that contain large vacuoles and glycogen.
• It tissues such as cardiac myocytes.
• In contrast to smooth and skeletal muscle MLCKs, cMLCK expression is restricted to cardiac myocytes.
• Cardiac troponin is another ROCK1 substrate that upon phosphrylation causes reduction in tension in cardiac myocytes.
• This stabilizes the electrochemical potential of cardiac myocytes, thereby preventing the development of fatal arrhythmias.
• In general, this is caused by dysfunction or destruction of cardiac myocytes or their molecular components.
• The action of azimilide is directed to the different currents present in atrial and ventricular cardiac myocytes.
• Phosphorylation of these channels increases their permeability to calcium and increases the contractility of their respective cardiac myocytes.
• Weaker contractions will lead to more blood flow in the coronary arteries, which will help the ischemic cardiac myocytes.
• Their working mechanism is based on binding to sodium channels, which leads to increased excitation especially in cardiac myocytes.
• The delayed rectifier potassium ion current is largely responsible for the repolarization of ventricular cardiac myocytes by permitting potassium efflux.
• JZTX-XI reduces the peak sodium current amplitude of sodium channels expressed in cardiac myocytes and slows down current inactivation.
• EAD is an abnormal depolarization and increase in action potential frequency that occurs in cardiac myocytes before normal repolarization is complete.