Secondary active transport model. The binding of a sodium ion to the transporter produces an allosteric alteration in the affinity of the solute binding site at the extracellular surface of the membrane. The absence of sodium binding at the intracellular surface, due to the low intracellular sodium concentration, reverses these changes, producing a low-affinity binding site for the solute, which is then released. [Q]
Movement of Molecules Across Cell Membranes CHAPTER SIX
in some cases it can be another ion such as bicarbonate, chloride, or potassium. The binding of an ion to the secondary active transporter produces similar changes in the transporter as occur in primary active transport, namely, (1) altering the affinity of the binding site for the transported solute, or (2) altering the rate at which the binding site on the transport protein is shifted from one surface to the other. Note, however, that during primary active transport, the transport protein is altered by covalent modulation resulting from the covalent linkage of phosphate from ATP to the transport protein; in secondary active transport, the changes are brought about through allosteric modulation as a result of ion binding (Chapter 4).
There is a very important indirect link between the secondary active transporters that utilize sodium and the primary active sodium transporter, the Na,K-ATPase. Recall that the intracellular concentration of sodium is much lower than the extracellular sodium concentration because of the primary active transport of sodium out of the cell by Na,K-ATPase. Because of the low intracellular sodium concentration, few of the sodium binding sites on the secondary active-transport protein are occupied at the intracellular surface of the transporter. This difference provides the basis for the asymmetry in the transport fluxes, leading to the uphill movement of the transported solute. At the same time, the sodium ion that binds to the transporter at the extracellular surface moves downhill into the cell when the transporter undergoes its conformational change.
To summarize, the creation of a sodium concentration gradient across the plasma membrane by the primary active transport of sodium is a means of indirectly "storing" energy that can then be used to drive secondary active-transport pumps linked to sodium. Ultimately, however, the energy for secondary active transport is derived from metabolism in the form of the ATP that is used by the Na,K-ATPase to create the sodium concentration gradient. If the production of ATP were inhibited, the primary active transport of sodium would cease, and the cell would no longer be able to maintain a sodium concentration gradient across the membrane. This in turn would lead to a failure of the secondary active-transport systems that depend on the sodium gradient for their source of energy. Between 10 and 40 percent of the ATP produced by a cell, under resting conditions, is used by the Na,K-ATPase to maintain the sodium gradient, which in turn drives a multitude of secondary active-transport systems.
As discussed in Chapter 4, the energy stored in an ion concentration gradient across a membrane can also be used to synthesize ATP from ADP and Pj. Electron transport through the cytochrome chain produces a hydrogen-ion concentration gradient across the inner mitochondrial membrane. The movement of hydrogen ions down this gradient provides the energy that is coupled to the synthesis of ATP during oxidative phos-phorylation—the chemiosmotic hypothesis.
As noted earlier, the net movement of sodium by a secondary active-transport protein is always from high extracellular concentration into the cell, where the concentration of sodium is lower. Thus, in secondary active transport, the movement of sodium is always downhill, while the net movement of the actively transported solute on the same transport protein is uphill, moving from lower to higher concentration. The movement of the actively transported solute can be either into the cell (in the same direction as sodium), in which case it is known as cotransport, or out of the cell (opposite the direction of sodium movement), which is called countertransport (Figure 6-14). The terms "symport" and "antiport" are also used to refer to the processes of cotransport and countertransport, respectively.
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This ebook provides an introductory explanation of the workings of the human body, with an effort to draw connections between the body systems and explain their interdependencies. A framework for the book is homeostasis and how the body maintains balance within each system. This is intended as a first introduction to physiology for a college-level course.