Facilitated Diffusion and Active Transport

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Physiology 500A

Membrane Transport

Lectures #5 and #6


Berne & Levy, Principles of Physiology, 2nd edition pp. 12-17

Berne & Levy, Physiology, 4rd edition pp. 13-19

Cell Physiology Sourcebook, 3ed edition, pp. 249-259


• Know the similarities and difference between simple diffusion, facilitated diffusion, primary active transport, co-transport and counter-transport.

• Be able to provide examples of each type of transport

• Understand the energy source which drives each type of transport

Facilitated Diffusion/Active Transport

Understanding carrier-mediated transport is important to a basic understanding of how cells, and therefore organisms, work. Most biological membranes are virtually impermeable to hydrophilic molecules. All essential nutrients (e.g. ions, glucose, amino acids) must be brought into the cell via some sort of regulated transport mechanism rather than via diffusion.

The intracellular concentration of many water soluble solutes (e.g. glucose, ions) is very different than the extracellular concentrations. These gradients provide the energy available to the cell for carrier-mediated transport and other cellular processes. In this discussion of transport processes, we will talk about how this energy is used, as well as how these gradients are set up and maintained using transport processes.

There are two general characteristics of carrier-mediated transport. The first is that all carriers display a high degree of structural specificity of the substrate that is transported. In other words, a transporter may have a high affinity for the L-stereoisomer of an amino acid, but not the D-stereoisomer. Secondly, all carrier-mediated processes exhibit saturation. This means that the rate of transport will approach a maximum as the concentration of substrate is increased (Figure 5.1). This contrasts from a simple diffusion process as diffusion is characterized by a linear, non-saturating transport rate (dashed line in Figure 5.1).

This contrasts from a simple diffusion process as diffusion is characterized by a linear, non-saturating transport rate (dashed line in Figure 5.1).

Saturation kinetics reflects the fact that there is a fixed number of transport molecules available to carrier substrates across a cell membrane. At saturation, all the carrier sites are occupied and further increasing the concentration of solute will have no effect on the transport rate. A consequence of a limited number of binding sites is competitive inhibition of substrates or solutes. This will happen when there are two solutes that can be transported by a single transport molecule. The presence of a second substrate that can occupy binding sites on the carrier will prevent the first from being transported.

An example of this is the Na+/glucose transporter found in the small intestine. This carrier will transport either glucose or galactose equally well, with similar rate of maximal transport. If both sugars are present, however, the rate of glucose transport will be decreased because galactose will be occupying some of the transport sites.



Carrier-Mediated Transport

The movement of certain classes of molecules across cell membranes clearly does not follow the equations predicted for either

  • (a) Fick-type diffusion through the bulk lipid phase of the membrane or
  • (b) passage through pores or channels. A large fraction of these transport phenomena can be interpreted in terms of a hypothetical "carrier" present in the membrane, which accepts the substance under study at one side of the membrane, and delivers it to the other.

At one time it was thought that “carrier proteins” that shuttled back and forth across the membrane, rather like a ferryboat in fact, mediated permeation of hydrophilic molecules. A few "carrier molecules" have been found such as the antibiotic valinonycin that wraps around K+ ions and ferries them across the membrane. It is now generally recognized that transport proteins usually span the entire membrane and that the mechanism of operation is to bind substrate on one side, undergo a conformational change, and release it on the other. This is called an "alternating access" mechanism of transport (Figure 5.2). Examples are known that include all of the four types of transport activity that we will discuss.

FACILITATED DIFFUSION or Passive Carrier-Mediated Transport: (also called uniport)

Certain molecules traverse cell membranes at a rate considerably higher than would be expected from a simple consideration of membrane structure. For example, glucose cannot penetrate lipid bilayers very readily, yet it crosses red blood cell membranes very rapidly in passive fashion. Starved erythrocytes take up glucose very rapidly from a glucose-rich medium, yet lose it equally rapidly when placed in a glucose-free solution. The presence of other sugars with similar structure may reduce glucose entry into the cell (i.e. competitive inhibition) and certain substances (e.g. thiol-blocking agents) may abolish it altogether. These observations are inconsistent with simple diffusion processes.

Facilitated transport mechanisms are present in the membranes of all cells. Common features include

  • 1) integral membrane spanning proteins,
  • 2) substrate specificity,
  • 3) inhibition by substrate analogues,
  • 4) transport rate saturation and
  • 5) alternate side-to-side re-orientation of substrate associate binding site.

One important feature of carrier mediated facilitated diffusion mechanisms is that the carrier protein itself is not altered during the transport process. Only thermal energy is required for the conformational change of the protein. The two main features of facilitated transport are the association of the substrate with the carrier molecule on one side of the membrane and dissociation on the other. Figure 5.2 shows a conceptual and kinetic model of facilitated diffusion. The direction of transport is determined by the concentration gradient of the substrate. If the extracellular concentration of the substrate (e.g. glucose) is high and the intracellular concentration is low, then the carrier protein will facilitate glucose transport from outside to inside. The opposite is also true. If the glucose concentration is higher on the inside of the cell than on the outside, then glucose will move out of the cell via the carrier.

Several carrier proteins mediating facilitated diffusion of glucose have been identified and cloned. All consist of approximately 500 amino acids with a high degree of homology including 12 putative transmembrane spanning regions (Figure 5.3).

Facilitated diffusion may mediate transport of non-electrolytes such as glucose or charged solutes such as organic anions or cations. The transport of electrolytes will result in a net transfer of charge across the membrane and thus can influence the membrane potential of the cell. Additionally, electrogenic facilitated transport will have a reversal potential.Thus its ability to transport charged solutes will be influenced (at steady–state) by the membrane potential. Thus, membrane potential must be considered an additional driving force when determining the direction of transport.

Facilitated Transport of Glucose


Glucose is the primary energy source for most cells of the body. The diffusion of glucose across cell membranes is very slow. Facilitated diffusion makes glucose transport faster and thus feasible to address the energy needs of the body. Cells of adult humans contain three distinct but homologous isoforms of the glucose transporter. Examples of D-glucose transporter are shown in Table I.

In adipocytes and muscle cells, insulin increases the rate of glucose transport by promoting the insertion of additional glucose transporter proteins into the plasma membrane. A pool of glucose transporters is maintained in the endoplasmic reticulum. This pool of proteins is transferred to the plasma membrane via vesicle fusion in the presence of insulin (Figure 5.4).

Pancreatic beta cells secrete very little insulin in response to elevated blood levels of glucose in type I diabetes mellitus, or insulin-dependent, diabetes. The rate-limiting step of glucose metabolism is the transport of glucose into muscle and adipose cells. Glucose transport into these cells is very slow in the absence of insulin. These cells must turn to other fuels, such as fats, to satisfy their energy needs in type I diabetes.

In some cells, glucose metabolism is regulated by metabolic demands. Decreased levels of ATP and increased levels of ADP and AMP in red cells and certain neurons stimulate glucose transport. Anoxia in cardiac muscle and exercise in skeletal muscle also stimulate glucose transport. These responses may involve the insertion of additional transporters into the plasma membrane, but most of the response is attributable to the stimulation of the existing transporters in the membrane.

Channel vs. transporters

Transport mediated by ion channels and facilitated transporters are passive. Both means of transport share characteristics of inhibition and saturation. The transport rate of ion channels, however, is orders of magnitude higher than most carrier mediated transport mechanisms because ion channel proteins do not have to undergo major conformational changes. A correlated point is that both sides of an ion channel are accessible at all times, whereas a binding site on a carrier molecule is available only to one side of the membrane at a time. In addition, the rate-limiting step for substrate translocation in an ion channel is the association and dissociation of the ion with the channel protein, whereas the rate limiting step of a carrier molecule is usually the conformational change allowing substrate translocation.

Active Transport

Active transport refers specifically to carried-mediated transport process in which the chemical energy (e.g., ATP hydrolysis) is directly consumed for the translocation of substrates across the membrane. Active transport also refers to the transfer of a charged substrate against combined electrical and chemical (i.e. concentration gradient) driving forces.

Active transport works against simple diffusion down a concentration gradient. Active transport processes perform work. The energy for this work comes from the hydrolysis of ATP and/or ion concentration gradients. Active transport processes can be inhibited by any process or compound (i.e. poison) that inhibits metabolism. There are two classes of active transport: Primary active transport which uses ATP to move a substrate against its concentration gradient and secondary active transport in which transport against a concentration gradient is not coupled directly to ATP hydrolysis, but uses instead the dissipation of the free energy of an ion (e.g., Na+) whose electrochemical gradient was established by active transport.


This class of carrier mediated transporters is responsible for moving a substrate against a concentration gradient or, if the substrate is charged, against a concentration gradient combined with difference in electrical potential. ATP hydrolysis is required.

The best studied examples of this type of transport are:


  • The Na+/K+ ATPase (Na+/K+ pump): This carrier mechanism is found in virtually all cells of high animals and is responsible for maintaining low intracellular Na+ and high intracellular K+ concentrations. This protein is required for maintaining the membrane potential of mammalian cells. We will talk in more detail about this transporter, below.
  • Ca++ ATPase (Ca++ pumps): There are at least two types of Ca++ ATPases. The carrier protein found in the sarcoplasmic reticulum re-accumulates calcium into the sarcoplasmic reticulum (in muscle) or calcium storage vesicles (in other cells). The muscle pump has been cloned and sequenced. Its structure is known at a resolution of about 7 Å.The calcium pump found in the plasma membrane of many cells works slowly, but can establish extremely steep gradients. It is molecularly different from the SR calcium pump.
  • H+/K+ ATPase (proton pumps): There are several types of proton pumps. Proton (H+) pumps of intracellular organelles such as lysosomes, endosomes, certain secretory vesicles etc. Proton (H+) pumps appear to be electrogenic and different for different organelles. The electroneutral H+/K+ ATPase of gastric mucosal cells, responsible for proton secretion into the stomach. The proton ATPase of the collecting duct of the nephron, partly responsible for urinary acidification.

The proteins responsible for each of these activities have been identified. Each possesses ATPase activity in addition to specific ion ion binding sites.

Physiological Importance of the Sodium Pump

The sodium pump is ubiquitous. It maintains the Na+ and K+ concentration gradients normally present across most animal cell membranes. The function of electrically excitable cells, nerve and muscle, clearly depends on these gradients (Figure 5.5). In the kidney, large quantities of sodium are filtered by the glomerulus, and most of it must be reabsorbed in the tubules against an electrochemical gradient. In all cells of the body, sodium is continually leaking in, and must be pumped out by the sodium pump to maintain steady state. It has been estimated that as much as 50% of the basal O2 consumption (i.e., ultimately, ATP hydrolysis) results from the activity of sodium pumps. In fact, an interesting theory concerning the mechanism by which thyroid hormone regulates basal heat production in the body suggests that this is done by stimulation of sodium pumping.

Skeletal muscle cells placed in a potassium-free solution at low temperature (2 to 5˚C), will lose potassium and gain sodium from the external solution. If they are now placed in a solution containing potassium and the temperature is raised to room temperature (20˚C), the cells gain back the potassium lost and extrude the sodium ions gained in the cold, until the inside sodium concentration has been reduced to its characteristically low value. This outward transport of sodium ions is against an electrochemical gradient and hence is a demonstration of active transport.

Hodgkin and Keynes, in their initial study on Na+ and K+ movements in giant axons, showed that Na+ efflux and K+ influx were both markedly, but reversibly, inhibited by metabolic poisons (cyanide, azide and dinitrophenol); neither Na+ influx nor K+ efflux were affected. A second important observation was that the metabolism-dependent sodium efflux was markedly reduced when external potassium was removed. Caldwell et al. later showed that ATP was probably the direct source of energy for the sodium pump.

Blood to be used in transfusions is normally stored in the cold for periods of up to three weeks, during which time the erythrocytes lose potassium ions and gain sodium ions due to a decrease in ATP generation. Upon injection into the blood stream, the donor red blood cells rapidly gain potassium and lose sodium ions against the respective electrochemical gradients. This phenomenon can be duplicated in vitro by placing cold-stored red blood cells in a glucose-containing Ringer solution at body temperature

Properties of the Sodium Pump

There is a direct coupling between the uphill movements of K+ (influx) and of Na+ (efflux): active K+ influx requires the presence of intracellular Na+, and active Na+ efflux requires the presence of extracellular potassium.

Uphill ("active") transport requires ATP.

The action of the sodium pump may be diagramed as follows (Figure 5.6):


The evidence suggests that a protein contained within the membrane can, in the presence of ATP, bind Na+ at the inside surface of the membrane. Na+ gains access to the external surface, where it is exchanged for K+, which then gains access to the internal surface and discharged. (Indicated by arrows in the above figure)

Cardiotonic steroids inhibit the sodium pump.

The next significant advance came from Schatzmann's observation (1953) that the erythrocyte sodium pump was markedly inhibited by low concentrations (10-6 to 10-8 molar) of "cardiotonic (= cardioactive) steroids" (digitalis preparations such as "ouabain"). Subsequently, the sodium pumps in virtually all other animal tissues have been shown to have qualitatively similar cardioactive steroid sensitivity.

Digitalis drugs are among the half-dozen or so most useful drugs in the physician's armamentarium. They are invaluable in treatment of congestive heart failure, first discovered by William Withering nearly two centuries ago. Although the mechanism of action of digitalis is not completely understood, (partial) inhibition of the sodium pump is the only known action at therapeutic concentrations.

There exists a membrane-bound ATPase stimulated by Na+ and K+.

Since ATP is the ultimate energy source for active transport, it is expected that an ATPase enzyme catalyzing the hydrolysis of ATP be involved.

Skou (1957) who was awarded a Nobel Prize for his work in 1997 took a major step in this direction. Skou isolated crab nerve membrane fragments containing an ATPase activity with the following characteristics:


  • It is ATP-specific. Other nucleotides are relatively ineffective.
  • In the presence of optimal concentration of sodium, potassium and magnesium, ATP is hydrolyzed to ADP and inorganic phosphate.
  • The Na+-K+ dependent ATPase activity can be completely inhibited by cardiotonic steroids.

Similar ATPases have been found in a large variety of other tissues-virtually wherever it has been looked for. The Na+-K+ dependent ATPase activity in various tissues can usually be well correlated with the ability of the intact cells to transport Na+. For example there are two genetically different types of sheep, some with high-K+, low-Na+ red cells (= Hi K+ sheep) and some with low-K+, high-Na+ red cells (= Lo K+ sheep). It was found that the (Na+/K+) ATPase activity present in the membranes of these cells is proportional to the Na transport activity of intact cells.

Another type of correlation comes from the relative sensitivity to cardiotonic steroids. The rat, for example, is much more resistant to these drugs than the guinea pig is; and this is reflected both in the steroid-inhibited Na+ transport in intact tissues, and in the digitalis sensitivity of the Na+-K+ dependent ATPase. Also, unusually large doses of digitalis are required to enhance myocardial contractility in the rat, providing evidence for the correlation between sodium pump inhibition and inotropic action.

Since the initial work by Skou, a very large number of publications have appeared on this enzyme. Perhaps the most important subsequent achievement has been the demonstration, by Post and co-workers, of a phosphorylated enzyme intermediate formed during ATP hydrolysis.

The overall hydrolysis of ATP may be written:


ATP + H2O------->ADP + Pi

where Pi refers to inorganic phosphate. If Pi is radioactively labeled with P32, the label does not find its way into ATP or ADP. If ADP is labeled, the label gets into ATP. A reversible ATP ADP exchange reaction thus occurs and the following sequence is suggested:


(i) E + ATP E1 ~P + ADP

(ii) E1 ~P E2 - P

(iii) E2 - P E + Pi

Reaction (i) proceeds at very low Mg++ concentrations and requires the presence of Na+ ions. Reaction (ii) is practically irreversible, and is thought to be a molecular rearrangement whereby the affinity of the enzyme is changed from a sodium affinity to a potassium affinity. Reaction (iii) constitutes the final step in the hydrolysis and requires the presence of K+ ions. Cardioactive steroids inhibit it.

In addition, several laboratories have shown that the various steps and characteristics of the enzymatic reaction correlate well with what is already known about the properties of the sodium pump:


  • Sodium ions must be present inside the cells (shown in red blood cells) to facilitate ATPase activity. Potassium ions must be present on the outside of the cells.
  • External sodium ions and internal potassium ions are ineffective in this regard.
  • ATP and Mg++ must be present inside the cells, not outside.
  • Cardioactive steroids act on the outside but not the inside of the membrane.

Thus the elements of the crude extracted system are highly oriented in the intact transporting system. Figure 5.7 shows a simplified scheme involving these components.

The symbol E represents a membrane transport protein that is shown as having enzymatic activity at various places in the cycle. A ratio of 3 Na+ transported outwardly per 2 K+ transported inwardly is found experimentally. Such a pump results in the net extrusion of positive changes, and is therefore termed ""electrogenic"" (i.e., potential-producing) or ""rheogenic"" (i.e., current-producing).



Be able to understand and explain the difference between these two types of transport.


Transport Characteristics Simple Diffusion Facilitated Diffusion Primary Active Transport
linearity yes no no
saturation no yes yes
competition no yes yes
stereo-specificity no yes not applicable
symmetrical yes yes no
bi-directional yes yes Under certain circumstances


The steep sodium gradient across animal cell membranes resulting from activity of the Na – K pump, serves a fundamental purpose in addition to its obvious role in electrophysiology. The energy stored by the sodium pump in the transmembrane sodium electrochemical gradient is utilized to carry other substances into the cell (by means of a "co-transport" mechanism) or out of the cell (by means of "counter-transport" mechanisms) against their respective gradients. These mechanisms are also capable of "uphill" transport of substrate, but because they use the Na+ electrochemical gradient as a source of energy rather than ATP, they are called "secondary" active transport processes.

Secondary active transport processes are not directly coupled to metabolic energy (i.e. the break down of ATP). The energy driving this form of transport comes from coupling the movement of one substrate down its electrochemical gradient to the movement of another substrate against its concentration gradient (Figure 5.8). If the substrates are going in the same direction, this is called co-transport. If the substrates are going in opposite directions, it is called counter-transport. In both co-transport and counter-transport, both substrates must be bound following specific rules before transport will occur.

Most examples of co- and counter-transport use the energy stored in the Na+ gradient that has been created or maintained by the Na+/K+ ATPase. Any ion concentration gradient, however, may be used to drive this type of transport. Two examples are the K+/Cl- co-transporter, found in the plasma membrane of many cells and the Cl-/HCO3- exchanger (anion exchanger), found in red blood cells

Na+-glucose Co-Transport Driven by the Sodium Gradient

The carrier for the Na+-glucose co-transporter is located on the lumenal membrane of the intestinal mucosa and renal proximal tubule cells. Glucose is transported ‘uphill’ using the energy of the Na+ concentration gradient. The Na+/K+ ATPase maintains the inward gradient of Na+. Poisoning the pump will ultimately inhibit the Na+-glucose co-transporter. Removing extracellular Na+ or glucose will also prevent co-transporter function. In other words, both substrates must be bound for transport to occur.

In severe diarrheal illnesses, oral re-hydration therapy must include both NaCl and glucose in addition to K+ and HCO3-. The absorption of NaCl and glucose in the small intestine drives the osmotic absorption of water and facilitates re-hydration.

Epithelial transport couples the activity of the Na+-glucose co-transporter, Na+/K+ ATPase, and facilitated transport of glucose in order to move glucose from the intestinal lumen into the blood stream. The key to understanding this system is in the polarity of the membranes. The Na+-glucose co-transporter exists only on the lumenal side of the cell and takes glucose from outside to inside the cell. The Na+/K+ ATPase that is located on the basalateral side of the cell maintains the Na+ gradient. Tight junctions between the epithelial cells prevent the mixing of the transport proteins between the lumenal and basalateral sides of the cell. The glucose transporter is located on the basalateral (blood) side of the cell and severs to move glucose from inside the cell to blood. Glucose will move from the lumen to the blood until the concentration of glucose in the blood becomes high enough to decrease the gradient. Amino acids and other sugars (e.g. galactose) also enter epithelial cells via Na+-driven co-transport.

Na+-Ca2+ Counter-Transport Driven by the Sodium Gradient

The Na+/Ca++ counter transport protein (or Na+/Ca++ exchanger) is found in many types of cells and provides an additional mechanism for controlling the level on intracellular Ca2+ The energy of the Na+ gradient is used to extrude Ca2+ from the cell.

The exchanger works according to the following rules: 1) It can bind either sodium or calcium; not both simultaneously, 2) The un-complexed transporter cannot change its conformation (i.e. transport ions across the membrane), 3) The transporter can change it conformation in either the sodium form or the calcium form. Note that there is a net charge movement with the exchange of Na+ for Ca++. This means that the activity of this exchanger will be electrogenic.

Intracellular Ca2+ concentration in heart cells is regulated by the Na+/Ca2+ exchanger located in the plasma membrane in addition to the Ca2+ ATPase located in the sarcoplasmic reticulum. These two proteins mediate the decrease in intracellular Ca2+ that occurs during diastole.

Sodium-proton (sodium-hydrogen) exchange.

Figure 10 shows examples of different Na+/H+ exchangers. These exchangers have similar rules of substrate association and dissociation as the Na+/Ca++ exchanger. The rules are: 1) It can bind either sodium or hydrogen, not both simultaneously, 2) The un-complexed transporter cannot change its conformation and 3) The transporter can change from outside-facing to inside-facing and back in either the sodium form or the hydrogen form. There is no net charge crossing the membrane so the membrane potential has no effect on ion transport (unlike the Na+/Ca++ exchanger).

Most cells express a Na+/H+ exchanger. This protein prevents the acidification of the cytosol. When the pH of the cytosol is normal (~7.2-7.4), the affinity of the exchanger for H+ is low and there is little transport activity. Exchanger activity increases as the cytosol becomes more acidic. Again, the Na+ gradient, maintained by the Na+/K+ ATPase provides the energy to transport H+ out of the cell.

Treatment of cells with certain growth factors, tumor promoters and mitogens results in phosphorylation of the Na+/H+ exchanger. This increases its affinity for H+, resulting in increased transport activity at normal pH and persistent alkalization of the cytosol. Apparently, activation of this exchanger is required for stimulation of cell division by mitogens. The mechanism by which alkalization of the cytosol results in stimulating mitosis is not understood.

So, how much of a concentration gradient can be developed by Secondary Active Transport?

The Na+/Ca++ exchanger moves 3 Na+ ions in for every Ca++ moved outward.

The ability of the exchanger to move Ca++ out is dependent on the relative concentration gradients of the two ions, in addition to the membrane potential. The extruding ability is given by the following formula:

Where m = the number of Na+ ions moved per Ca2+ and n = the number of net positive changes moved into the cell per Ca2+ moved out of the cell. In this case, m = 3 and n= 1. Remember that Vm has its usual meaning of membrane potential.

The parameter m represents the number of Na+ ions translocated inward per substrate molecule. The parameter ‘n’ represents the number of net positive charges that "fall down" the electrical gradient established by the membrane potential. ‘n’ is also a measure of whether the transporter is electrogenic or not. Hence, in the diagram above there is a 10-fold concentration gradient for Na+ and 3 Na+ ions enter per Ca++. The chemical part of the Na+ electrochemical gradient can extrude Ca++ up a concentration gradient of 10^3. How much "extruding power" is available in the electrical gradient? If each Na+ falls down 60 mV, their extruding ability is 10^3; however, when one Ca++ is raised from -60 mV to zero mV, two positive charges have to be moved out. The net extruding power from the electrical gradient is, therefore

electrical extruding power = 10^3 x 10^-2 = 10^1

and the overall electrical plus chemical extruding power is overall extruding power = Na+ chemical x net electrical = 10^3 x 10^1 = 10^4

Thus if Vm= -60 mV, and there is 150 mM Na+ and 1 mM Ca++ outside the cell and 15 mM Na+ inside the cell, what is the intracellular concentration of Ca++?

Answer:0.1 µM Ca++

Whether we obtain concentrating or extruding ability depends on whether the substance is co- or counter- transported, respectively.

In the case of a 3Na+/I- iodide co-transporter show at right, the concentrating ability = 10^3 x 10^(3-1) = 10^5.

Note: the charge on anion is opposite that of cations! Taking an anion out of the cell is equivalent to taking a cation in. Try the problem to the right. You should get

[I-]i/ [I-]o=105 (concentrating ability) Therefore: [I-]I = 0.1M

In all the examples we have had so far, the Na+ gradient has been the driving force for co- or counter transport. This does not have to be the case. For the K+/Cl- co-transporter, the driving force would be K+ and the concentration gradient for K+ would be substituted for Na+:


[S]i/[S]o= ([K]o/[K]i)m • 10(-nVm/60)

This transporter is electroneutral so that n = 0. And there is one K+ ion moved for every Cl- moved, so m = 1. Therefore:


[S]i/[S]o= 0.1 and [Cl-]I = 15 mM

Similarly, the driving force for the Cl-/HCO3- exchanger is the chloride gradient.


[S]o/[S]i = ([Cl]o/[Cl]i)m • 10(-nVm/60)

Again, this transporter is electroneutral so that n = 0. And there is one Cl- ion moved for every HCO3- moved, so m = 1.

If you work through the problem shown at right, you should find that the extruding ability is [HCO3-]o/ [HCO3-]i=101 (extruding ability), making the [HCO3-]I =10 mM.


Make sure to understand the similarities and difference between the transport processes discussed. Some of the important characteristics of these processes are summarized in Table II.


Transport Type Electro-chemical Gradient Carrier-Mediated Metabolic Energy Uses the energy of C- or Counter Transported ion
CO-TRANSPORT Uphill Yes Indirect Yes, same direction
COUNTER-TRANSPORT Uphill Yes Indirect Yes, opposite direction


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