Thirty seconds to save a life
Before your cerebral cortex has finished consciously processing a sudden danger, something has already happened in your body: pupils dilated, heart beating faster and harder, bronchi opened, muscles receiving more blood and glucose. That coordination is adrenaline (epinephrine), released by the adrenal medulla in response to sympathetic nervous system activation.
Structure: dopamine with two modifications
Adrenaline (C₉H₁₃NO₃) is dopamine with: (1) a –OH group on the β-carbon of the ethylamine chain, and (2) an N-methyl group on the terminal nitrogen. The β-carbon is a stereogenic center — the physiologically active form is (R)-(−)-adrenaline, ~10× more potent than its enantiomer at α receptors.
Adrenergic receptors: α and β
α₁ (smooth muscle): vasoconstriction → raised blood pressure; skin blanches. β₁ (heart): positive chronotropy and inotropy → faster, stronger heartbeat. β₂ (bronchial smooth muscle): bronchodilation → airways open; also vasodilation in skeletal muscle. β₃ (adipose tissue): lipolysis → fatty acids mobilized as fuel. The distribution of α vs β effects depends on adrenaline concentration: low doses → β₂ dominates (vasodilation); high doses → α₁ dominates (vasoconstriction).
Three critical medical uses
Anaphylaxis: Simultaneous reversal of bronchospasm (β₂), systemic vasodilation/shock (α₁), and airway edema. The EpiPen contains 0.3 mg — enough to gain the critical minutes until hospital care. Cardiac arrest: IV adrenaline (1 mg every 3–5 min) during CPR increases coronary and cerebral perfusion pressure. Local anesthesia: Adding adrenaline to local anesthetics causes local vasoconstriction, slowing systemic absorption and prolonging anesthetic duration.