Potassium is a charged mineral that is very important for proper electrical conduction in the body. As such, it is particularly important for nerve and muscle cells. Its levels are very tightly regulated in the body. One source of regulation is the hormone aldosterone. It is important to consult with a physician for the diagnosis and treatment of medical conditions.
Potassium is ingested in the diet and absorbed through special protein channels in the cells lining the intestinal wall. The oral route helps slow the rate of increase in the blood, so that the kidneys can handle the increase in potassium. Once in the body, potassium is distributed differently inside and outside of cells, with a high concentration inside cells and a low concentration outside them. Aldosterone signals the kidneys to excrete potassium into the urine.
The adrenal glands are paired organs that sit above the kidneys in the back. The adrenal cortex, or outer layer, produces steroid hormones from cholesterol. Signals from the blood cause the kidneys to make more or less aldosterone.
In addition to signaling the kidneys to excrete potassium, aldosterone promotes the absorption of sodium. It does this by signaling kidney cells to produce and activate pumps that control the level of minerals in the urine and blood. The results include lowered potassium, while the increased sodium increases the water content of the blood and raises the blood pressure.
Disorders and Drugs
The drugs amiloride and spironolactone oppose aldosterone. They have the effect of lowering the blood pressure and raising potassium levels. A low level of aldosterone is called hypoaldosteronism, and is often caused by problems with the adrenal gland. Hyperaldosteronism, or high aldosterone levels, can result from an overgrowth of the adrenal glands or improper signaling from blood hormones.
- “Physiology”; Linda S.Costanzo; 4th Ed 2008
- “Robbins and Cotran Pathologic Basis of Disease”; Vinay Kumar, et al.; 8th Ed 2009
- “Basic and Clinical Pharmacology”; Bertram Katzung, et al.; 11th Ed 2009