Membrane transport
Also known as: diffusion, facilitated diffusion, osmosis, tonicity, active transport, Na+/K+-ATPase, sodium-potassium pump, symport, antiport, endocytosis, exocytosis, phagocytosis, pinocytosis
The ways substances cross the plasma membrane: passively down their gradients (simple and facilitated diffusion, osmosis), actively against them using ATP or ion gradients, and in bulk by endocytosis and exocytosis.
Overview
Passive transport needs no metabolic energy. In simple diffusion, small non-polar molecules (O₂, CO₂, N₂, steroid hormones, fatty acids, ethanol, urea slowly) cross the lipid bilayer directly; the rate is proportional to the concentration gradient, surface area and permeability, and inversely to membrane thickness (Fick's law). Facilitated diffusion uses proteins: channels form aqueous pores (often gated by voltage, ligand or stretch) and move up to ≈10⁶–10⁸ ions per second; carriers (uniporters such as the GLUT glucose transporters) bind the solute and change conformation, are slower (≈10²–10⁴ molecules per second) and saturate (Vmax, Km), show specificity and can be competitively inhibited. Osmosis is the diffusion of water — through the bilayer and much faster through aquaporins — toward the side of higher solute concentration. Tonicity describes the effect of a solution on cell volume: in an isotonic solution (≈290 mOsm/kg; 0.9 % NaCl) cells keep their volume; in a hypotonic solution they swell and may lyse; in a hypertonic solution they shrink (erythrocytes crenate).
Active transport moves solutes against their electrochemical gradient. Primary active transport is driven directly by ATP hydrolysis: P-type ATPases such as the Na⁺/K⁺-ATPase (3 Na⁺ out, 2 K⁺ in per ATP), SERCA and plasma-membrane Ca²⁺-ATPases and the gastric H⁺/K⁺-ATPase; V-type H⁺-ATPases acidify lysosomes and endosomes; ABC transporters (e.g. MDR1/P-glycoprotein, which pumps drugs out of cancer cells). Secondary active transport uses the energy stored in the Na⁺ gradient: symporters move both solutes in the same direction (SGLT1 — 2 Na⁺ with 1 glucose; SGLT2 — 1 Na⁺ with 1 glucose; Na⁺–amino-acid and Na⁺–K⁺–2Cl⁻ cotransporters), antiporters (exchangers) move them in opposite directions (Na⁺/Ca²⁺ exchanger — 3 Na⁺ in, 1 Ca²⁺ out; Na⁺/H⁺ exchanger).
Vesicular (bulk) transport moves macromolecules and particles. Endocytosis includes phagocytosis ("cell eating" of particles ≥ ≈0.5 µm by macrophages and neutrophils, driven by actin pseudopodia), pinocytosis ("cell drinking" of extracellular fluid, including macropinocytosis and caveolae) and receptor-mediated endocytosis, in which ligands (LDL, transferrin, insulin) bound to receptors cluster in clathrin-coated pits that pinch off with the help of dynamin. Exocytosis releases vesicle contents and inserts vesicle membrane into the plasma membrane. Transcytosis combines both to carry material across an epithelium or endothelium.
Parts & subdivisions
- Simple diffusionDown the gradient directly through the bilayer; non-saturable.
- Facilitated diffusionVia channels or carriers (e.g. GLUT1–4); carriers saturate.
- Osmosis and tonicityWater movement through bilayer and aquaporins; iso-, hypo-, hypertonic.
- Primary active transportATP-driven pumps: Na⁺/K⁺-ATPase, Ca²⁺-ATPases, H⁺/K⁺-ATPase, ABC transporters.
- Secondary active transportCoupled to the Na⁺ (or H⁺) gradient: symport (SGLT) and antiport (NCX, NHE).
- Phagocytosis, pinocytosis, receptor-mediated (clathrin) endocytosis.
- Vesicle fusion with the plasma membrane; constitutive or regulated.
Function
- Nutrient uptake and waste removal.
- Generation of ion gradients and the membrane potential.
- Regulation of cell volume and pH.
- Absorption and secretion by epithelia.
- Uptake of macromolecules and pathogens; secretion of products.
- Physiology
The Na⁺/K⁺-ATPase is electrogenic (net export of one positive charge per cycle) and consumes roughly a quarter to a third of a typical cell's resting ATP — far more in neurons and renal tubule cells. By keeping intracellular Na⁺ low it prevents osmotic swelling (the "pump-leak" balance) and powers secondary transport of glucose, amino acids, Ca²⁺ and H⁺. GLUT4 (skeletal muscle, adipose tissue) is the insulin-regulated glucose transporter; GLUT2 (liver, pancreatic β cells, basolateral enterocytes) has a high capacity and low affinity.
Clinical significance
Cardiac glycosides
Digoxin inhibits the Na⁺/K⁺-ATPase → intracellular Na⁺ rises → less Ca²⁺ is extruded by the Na⁺/Ca²⁺ exchanger → more Ca²⁺ stored in the sarcoplasmic reticulum → stronger contraction. Toxicity is increased by hypokalaemia.
Drugs targeting transporters
SGLT2 inhibitors (gliflozins) cause glycosuria in diabetes; loop diuretics block NKCC2, thiazides block NCC; proton-pump inhibitors block the gastric H⁺/K⁺-ATPase. Oral rehydration solution exploits SGLT1 glucose–Na⁺ cotransport, which remains intact in cholera.
Intravenous fluids and tonicity
0.9 % NaCl is isotonic; 5 % dextrose is iso-osmotic on infusion but effectively hypotonic once the glucose is metabolised — rapid infusion of hypotonic fluids can cause cerebral oedema, and too-rapid correction of chronic hyponatraemia causes osmotic demyelination.
Mnemonics
Pump stoichiometry
"Pump 3 out, 2 in" — per ATP the Na⁺/K⁺-ATPase expels 3 Na⁺ and takes up 2 K⁺; the net loss of one positive charge per cycle makes it electrogenic.
Test yourself
SGLT1 in intestinal enterocytes is an example of:
- Facilitated diffusion
- Primary active transport
- Secondary active transport (symport)
- Receptor-mediated endocytosis
Answer: Secondary active transport (symport)
SGLT1 couples the downhill entry of 2 Na⁺ to uphill entry of glucose (or galactose). The Na⁺ gradient is maintained by the basolateral Na⁺/K⁺-ATPase; glucose leaves via GLUT2 by facilitated diffusion. This is the basis of oral rehydration solution.
Compiled from standard anatomy and physiology references — see the Cells & Tissues sources. For education only; not medical advice.