Organisms respond to changes in their internal and external environments
Homeostasis and the kidney
Homeostasis keeps internal conditions within narrow limits using negative feedback: a receptor detects a change, a coordinator (e.g. hypothalamus) triggers effectors that reverse it. Thermoregulation: vasodilation, sweating (too hot); vasoconstriction, shivering, raised metabolism (too cold). The liver deaminates excess amino acids, making urea. In the nephron: ultrafiltration in the glomerulus (high hydrostatic pressure; basement membrane and podocytes filter out cells and proteins); selective reabsorption in the proximal convoluted tubule (all glucose, most water and ions; microvilli, many mitochondria, co-transport); the loop of Henle creates a high solute concentration in the medulla (ascending limb pumps out Na⁺/Cl⁻, impermeable to water); the collecting duct reabsorbs water by osmosis. ADH from the posterior pituitary makes collecting-duct cells insert aquaporins, so more water is reabsorbed when blood ψ is low.
≈ 55 minNerve impulses and synapses
At rest (about −70 mV), the Na⁺/K⁺ pump moves 3 Na⁺ out and 2 K⁺ in; the membrane is more permeable to K⁺, which leaks out. A stimulus opens voltage-gated Na⁺ channels; Na⁺ rushes in: depolarisation to about +40 mV. Na⁺ channels close and K⁺ channels open: repolarisation, overshooting (hyperpolarisation). The refractory period ensures one-way, discrete impulses. Action potentials are all-or-nothing; stimulus strength is coded by frequency. Myelin (Schwann cells) insulates the axon so impulses jump between nodes of Ranvier (saltatory conduction), much faster. Speed also rises with axon diameter and temperature. At a cholinergic synapse, Ca²⁺ enters the presynaptic knob, vesicles release acetylcholine by exocytosis; ACh diffuses and binds receptors, opening Na⁺ channels; acetylcholinesterase breaks it down. Synapses allow summation, one-way transmission and inhibition.
≈ 55 minBlood glucose control
Blood glucose is kept near 5 mmol dm⁻³ by the islets of Langerhans in the pancreas. High glucose: β cells release insulin, which binds receptors on liver, muscle and fat cells; more GLUT4 transporters move to membranes; glucose is converted to glycogen (glycogenesis) and fat, and respiration increases. Low glucose: α cells release glucagon, which binds liver receptors; via the second messenger cyclic AMP and an enzyme cascade (protein kinase), glycogen is broken down (glycogenolysis) and glucose is made from amino acids and glycerol (gluconeogenesis). Adrenaline also raises glucose via cAMP. Type 1 diabetes: no insulin (autoimmune), treated with insulin injections. Type 2: cells less responsive to insulin, linked to obesity; treated with diet, exercise and drugs. Glucose is measured with test strips/biosensors using glucose oxidase.
≈ 45 minMuscle contraction and plant responses
Skeletal muscle fibres contain myofibrils made of repeating sarcomeres (Z line to Z line): thin actin and thick myosin filaments overlap. At the neuromuscular junction, ACh depolarises the sarcolemma; the impulse travels down T-tubules; the sarcoplasmic reticulum releases Ca²⁺. Ca²⁺ binds troponin, moving tropomyosin off the binding sites on actin. Myosin heads bind (cross-bridges), perform the power stroke (releasing ADP + Pᵢ), then ATP binds to detach them and is hydrolysed to recock the head. Actin slides over myosin: the I band and H zone shorten; the A band stays the same. Phosphocreatine regenerates ATP rapidly. Plants: auxin (IAA) causes cell elongation (acid growth) and phototropism; gibberellin causes stem elongation and stimulates amylase in seed germination; abscisic acid closes stomata in drought; the Venus fly trap closes by rapid changes in turgor after two hair touches.
≈ 55 min