Secondary active transport

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secondary active transport

In secondary active transport, in contrast to primary active transport, there is no direct coupling of ATP; instead, the electrochemical potential difference created by pumping ions out of the cell is used. [1]

The three main forms of this are uniport, counter-transport (antiport) and co-transport (symport).

Counter-transport

In counter-transport two species of ion or other solutes are pumped in opposite directions across a membrane. One of these species is allowed to flow from high to low concentration which yields the entropic energy to drive the transport of the other solute from a low concentration region to a high one. An example is the sodium-calcium exchanger or antiporter, which allows three sodium ions into the cell to transport one calcium out.

Many cells also possess a calcium ATPase, which can operate at lower intracellular concentrations of calcium and sets the normal or resting concentration of this important second messenger. But the ATPase exports calcium ions more slowly: only 30 per second versus 2000 per second by the exchanger. The exchanger comes into service when the calcium concentration rises steeply or "spikes" and enables rapid recovery. This shows that a single type of ion can be transported by several enzymes, which need not be active all the time (constitutively), but may exist to meet specific, intermittent needs.

Co-transport

Co-transport uses the downhill movement of one solute species from high to low concentration to move another molecule uphill from low concentration to high concentration (against its electrochemical gradient).

An example is the glucose symporter SGLT1, which co-transports one glucose (or galactose) molecule into the cell for every two sodium ions it imports into the cell. This symporter is located in the small intestines, trachea, heart, brain, testis, and prostate. It is also located in the S3 segment of the proximal tubule in each nephron in the kidneys [2]. Its mechanism is exploited in glucose rehydration therapy and defects in SGLT1 prevent effective reabsorption of glucose, causing familial renal glucosuria[3].

References

  1. Essentials of Human Physiology by Thomas M. Nosek. Section 7/7ch05/7ch05p12.
  2. Wright EM. (2001) "Renal Na+-glucose cotransporters", Am J Physiol Renal Physiol, 280:F10–F18
  3. Wright EM, Hirayama BA, Loo DF. (2007) "Active sugar transport in health and disease", J Intern Med, 261:32–43




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