Sodium-Potassium-ATPase High Activity

Sodium-potassium-ATPase is a crucial enzyme responsible for transporting sodium (Na) and potassium (K) ions across the cell membrane. It is present in the plasma membrane of all animal cells and is also called pump. The terms 'pump' and 'enzyme' are often used interchangeably. The pump maintains a much higher concentration of potassium (and a much lower concentration of sodium) in the cytoplasm than exists outside the cell. This cation transport system is essential for cell function and plays a central role in the Na+, K+ balance of virtually all animals. Movements of ions into and out of a cell form the basis for the transmission of signals in the brain and heart as well as other tissues of the body that allow all animals to breathe, move, think, digest food and pretty much function in all respects. Most ion pumps transport different kinds of ions in opposite directions across cell membranes.

Critical Role of Potassium

Potassium is essential for the proper functioning of the heart, kidneys, muscles, nerves, and digestive system. Usually the food supplies all of the potassium needed. However, certain diseases (e.g., kidney disease and gastrointestinal disease with vomiting and diarrhea) and drugs, especially diuretics ('water pills'), remove potassium from the body.

Factors Affecting Sodium-Potassium-ATPase High Activity

Exercise

Exercise induces a loss of K+ from the muscle cells into the extracellular space, giving rise to an increase in blood K+. In man, hyperkalemia, or high blood potassium levels characterized by extreme weakness and soft paralysis, occurs during both dynamic and static exercise and is believed to play a role in the development of muscular fatigue. While the long-term control of plasma K+ concentrations depends ultimately on kidney function, achieved by increasing the concentration of Na+,K+ pumps in the cell membrane (for example, by thyroid hormones or training), it is skeletal muscle that plays the dominant role in its acute adjustment, by increasing the activity of the Na+,K+ pump (for example, by adrenaline;), or by increasing the concentration of Na+,K+ pumps in the cell membrane (for example, by thyroid hormones or training). These muscles represent the body's largest pool of K+ and Na+,K+ pumps, and therefore provide an enormous capacity for rapid Na+,K+ exchange.

Hyperthyroidism

Thyroid hormones largely determine the concentration of Na+,K+ pumps in skeletal muscle through a general endocrine effect. Hyperthyroidism gives rise to an increase in pump activity, while hypothyroidism (the most frequent thyroid disorder encountered in dogs) results in its decreased activity. Lack of magnesium can also lead to accumulation of intracellular sodium and loss of intracellular potassium.

Drugs

The sodium-potassium pump high activity is believed to underlie high blood pressure and it is the target of digoxin, one of the most widely prescribed drugs for heart disease. A closely related ion pump, the hydrogen-potassium pump, controls the production of stomach acid and is targeted by new antacid drugs, such as Prilosec.

Hereditary High-Potassium Erythrocytes with High Na, K-ATPase Activity

Erythrocytes, or red blood cells (RBCs), provide vital functions of oxygen transport, carbon dioxide transport and buffering of hydrogen ions. These functions require energy in the form of adenosine triphosphate (ATP) to keep the cells working.

Breeds at Risk

Some Japanese breeds such as Akita and Shiba Inu have erythrocytes with high potassium, low sodium concentrations, due to retention of Na, K-ATPase in mature erythrocytes, inherited as autosomal recessive trait. Some of these dogs have an increased concentration of reduced glutathione in their erythrocytes, which protects the cells against oxidative damage.³

References

1. Maria E. Everts. Potassium homeostasis during exercise in domestic species: the role of the sodium-potassium pump in skeletal muscle
2. Deadly Coral Toxin Exposes Ion Pump's Deepest Secret. ScienceDaily (Jan. 27, 2003)
3. Mary Anna Thrall, Dale C. Baker. Veterinary hematology and clinical chemistry