Abstract
In hypertensive humans and animals, intracellular calcium (Ca2+) has been found to be elevated in several cell types, including platelets, red blood cells, and smooth muscle cells. The messenger role of calcium requires its maintenance within cells at very low (submicromolar) ionic concentrations. This transcellular gradient is maintained by the reversible complexing of calcium to specific proteins. Intracellular free calcium can increase through an enhanced influx, release from intracellular stores, or a reduced efflux of calcium from the cell. Calcium channels are found to be increased in activity in some studies of hypertensive animals, but not in others. Sequestration of calcium within the cell has also been implicated in the increased cytosolic calcium in hypertension. Plasma membrane adenosine triphosphatases (ATPases) play a significant role in calcium extrusion; and the activity of these pumps has boon found to be decreased in several human and animal studies. A single cause of the cellular calcium alterations in hypertension is not completely clear.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 564-568 |
| Number of pages | 5 |
| Journal | Seminars in nephrology |
| Volume | 15 |
| Issue number | 6 |
| State | Published - Nov 23 1995 |
ASJC Scopus subject areas
- Nephrology