Ultrafiltration and selective reabsorption

The functional unit of the kidney is the nephron.

Ultrafiltration (in the Bowman’s capsule): the afferent arteriole is wider than the efferent arteriole, so a very high hydrostatic pressure builds up in the glomerulus. This forces water, glucose, amino acids, urea and mineral ions out through the fenestrations of the capillary endothelium, through the basement membrane — the actual molecular sieve — and between the podocytes. Blood cells and plasma proteins are too large to pass, so they remain in the blood.

Selective reabsorption (proximal convoluted tubule): about 85 % of the filtrate is reabsorbed here. All the glucose and amino acids are reabsorbed by co-transport with sodium ions; the Na⁺ is then actively pumped out of the cell into the blood, maintaining the gradient. The PCT epithelium is beautifully adapted: microvilli (huge surface area), many mitochondria (ATP for active transport), and a rich capillary supply. Water follows by osmosis.

Glucose in the urine means the co-transporters have been saturated — the renal threshold has been exceeded, which is why it is a classic sign of untreated diabetes.

Your turn — percentage reabsorbed

The loop of Henle, ADH and osmoregulation

The loop of Henle is a countercurrent multiplier. Sodium and chloride ions are actively pumped out of the ascending limb (which is impermeable to water) into the medulla. This makes the medulla tissue fluid increasingly negative in water potential the deeper you go. The descending limb is permeable to water, so water leaves it by osmosis, concentrating the filtrate as it descends.

The point of it all: the collecting duct passes back down through that same steep gradient, so water can be reabsorbed from it all the way along — producing urine that is more concentrated than the blood. A desert mammal with a very long loop of Henle can produce extremely concentrated urine.

Osmoregulation — negative feedback:

• The blood water potential falls (dehydration, salty meal).
• Osmoreceptors in the hypothalamus detect it and stimulate the posterior pituitary to release ADH.
• ADH makes the collecting duct more permeable to water by inserting aquaporins into its membrane.
• More water is reabsorbed → a small volume of concentrated urine → blood water potential rises back to normal.

Where in the nephron?

Tap a process, then tap where it happens.

Blood glucose and thermoregulation

Blood glucose is controlled by the islets of Langerhans in the pancreas:

• Too high → β cells release insulin → more glucose channels inserted into muscle and liver cell membranes, so glucose is taken up; glucose is converted to glycogen (glycogenesis) and to fat; respiration increases. Blood glucose falls.
• Too low → α cells release glucagon → the liver hydrolyses glycogen back to glucose (glycogenolysis) and makes glucose from non-carbohydrate sources (gluconeogenesis). Blood glucose rises.

Type 1 diabetes — the β cells are destroyed (autoimmune), so no insulin is made: treated with insulin injections. Type 2 — the cells become less responsive to insulin (receptor insensitivity): managed by diet, exercise and drugs.

Thermoregulation: the hypothalamus monitors blood temperature. Too hot — vasodilation of skin arterioles, sweating, hairs flat. Too cold — vasoconstriction, shivering, hairs erected, increased metabolic rate. Both are negative feedback.

Negative feedback

Phagocytosis and the specific immune response

Non-specific defences: skin, stomach acid, mucus and cilia, lysozyme, inflammation and phagocytosis. A phagocyte engulfs the pathogen into a phagosome, which fuses with a lysosome; hydrolytic enzymes digest it. The phagocyte then displays the antigens on its own surface as an antigen-presenting cell — the bridge between non-specific and specific immunity.

Cell-mediated (T cells): the T helper cell with the complementary receptor binds the presented antigen, is activated, and releases cytokines that stimulate phagocytes, T killer cells (which destroy infected cells) and B cells. T memory cells persist.

Humoral (B cells): the B cell with the complementary antibody binds the antigen; stimulated by T helper cytokines, it divides by mitosis (clonal selection and expansion) into plasma cells — which secrete large quantities of antibody — and B memory cells.

Antibody structure: a Y-shaped glycoprotein of four polypeptide chains, with two variable regions whose tertiary structure is complementary to one specific antigen, and a constant region. Antibodies agglutinate pathogens, neutralise toxins, and mark pathogens for phagocytosis (opsonisation).

Vaccination, immunity and HIV

The secondary response: memory cells mean that on re-infection, antibody is produced faster, in far greater quantity, and for longer — so the pathogen is destroyed before symptoms appear. That is immunity.

• Active immunity — you make your own antibodies and memory cells. Natural (infection) or artificial (vaccination). Slow to develop, but long-lasting.
• Passive immunity — you receive ready-made antibodies. Natural (placenta, breast milk) or artificial (antivenom). Immediate, but short-lived — no memory cells are made.

Herd immunity: if a high enough proportion of the population is vaccinated, the pathogen cannot spread, so even the unvaccinated are protected. Antigenic variation (as in influenza and HIV) is what defeats it: the surface antigens change, so existing memory cells no longer recognise the pathogen.

HIV binds CD4 receptors on T helper cells. As a retrovirus, it uses reverse transcriptase to make DNA from its RNA, which is inserted into the host genome. Replication destroys T helper cells; without them, neither the humoral nor the cell-mediated response can be activated properly, and the person becomes vulnerable to the opportunistic infections that define AIDS.

Why does HIV cripple the immune system?

Neurones, synapses and muscle

Resting potential (−70 mV): the Na⁺/K⁺ pump actively transports 3 Na⁺ out for every 2 K⁺ in, and the membrane is far more permeable to K⁺, which leaks back out. The inside is negative.

Action potential: at the threshold, voltage-gated Na⁺ channels open — Na⁺ floods in and the membrane depolarises to about +40 mV. The Na⁺ channels then close and voltage-gated K⁺ channels open, so K⁺ leaves and the membrane repolarises (with a brief hyperpolarisation). It is all-or-nothing: stimulus intensity is coded by the frequency of impulses, not their size. The refractory period ensures one-way conduction.

Myelination: myelin insulates the axon, so depolarisation can only occur at the nodes of Ranvier — the impulse jumps from node to node (saltatory conduction), which is much faster.

Synapse: Ca²⁺ enters the pre-synaptic knob → vesicles of acetylcholine fuse and release it → it diffuses across and binds receptors → Na⁺ channels open in the post-synaptic membrane → threshold reached → new action potential. Acetylcholinesterase then hydrolyses the transmitter.

Muscle contraction — sliding filament: Ca²⁺ released from the sarcoplasmic reticulum binds troponin, which moves tropomyosin off the actin binding sites. Myosin heads form cross-bridges, perform the power stroke, and ATP then binds to detach and re-cock each head. Actin and myosin slide past each other — the filaments themselves do not shorten.

Plants (4.3(a)): IAA (an auxin) made at the shoot tip is redistributed to the shaded side, where it causes cell elongation. The shaded side grows faster, so the shoot bends towards the light: positive phototropism. In roots, auxin inhibits elongation, producing positive gravitropism.

Nervous or hormonal?

Tap a feature on the left, then the system it describes.

Energy flow, GPP and NPP

An ecosystem is a community plus its abiotic environment. Energy enters as light and is fixed by producers; it flows through trophic levels and is ultimately lost as heat. Energy flow is one-way — unlike nutrients, which cycle.

Why so little gets through: not all of the previous level is eaten; not all that is eaten is digested — some is egested; energy is lost in excretion; and a great deal is released as heat in respiration, especially in endotherms. This is why food chains rarely have more than four or five links, and why a hectare of land feeds far more people if it grows crops than if it grazes cattle.

Your turn — net primary productivity

Your turn — energy transfer efficiency

The carbon and nitrogen cycles

Carbon cycle: CO₂ is removed from the atmosphere by photosynthesis and returned by respiration (of producers, consumers and decomposers), by combustion, and — over geological time — released from fossil fuels. Decomposers are essential: without saprobiotic bacteria and fungi, carbon would remain locked in dead organisms.

Nitrogen cycle — four processes, and you must be able to name the organisms:

• Nitrogen fixation — N₂ → ammonium. Free-living (Azotobacter) and symbiotic (Rhizobium, in the root nodules of legumes) bacteria.
• Ammonification — saprobiotic bacteria and fungi decompose proteins and urea in dead matter, releasing ammonium.
• Nitrification — an aerobic, two-step oxidation by nitrifying bacteria: ammonium → nitrite (Nitrosomonas) → nitrate (Nitrobacter). Nitrate is the form plants absorb.
• Denitrification — anaerobic denitrifying bacteria in waterlogged soil convert nitrate back to N₂, which is why farmers plough and drain to aerate the soil.

Succession and population growth

Succession: pioneer species colonise a hostile abiotic environment; they change it (weathering rock, adding humus) making it less hostile; new species colonise and out-compete them. Soil depth, biomass and biodiversity increase until a stable climax community is reached. Human activity (grazing, burning, mowing) can arrest it at a plagioclimax.

Population growth follows a sigmoid (S-shaped) curve:

• Lag phase — few individuals, acclimatising.
• Exponential (log) phase — resources are plentiful, so the population grows at its maximum rate.
• Stationary phase — the population reaches the carrying capacity. Density-dependent factors (competition for food, space and light; predation; disease; accumulation of waste) increase the death rate until it equals the birth rate.

Density-independent factors — a flood, a fire, an unusually cold winter — hit a population regardless of its size, and can crash it well below the carrying capacity.

Your turn — population growth rate

The nitrogen cycle

The big ideas to know

You have covered the whole of CCEA Unit A2 1 — ecosystems included. Press Finish to see your score.