Enzymes: blocking the worker
A receptor passes a message; an enzyme target does a job — it builds or breaks down a molecule. Many drugs work simply by sitting in an enzyme's pocket so the real substrate can no longer fit, an action called enzyme inhibition. A statin blocks the enzyme that makes cholesterol; an ACE inhibitor blocks the enzyme that makes a blood-pressure-raising hormone. The drug changes nothing by itself — it just stops a worker from working.
Channels and transporters: traffic control
An ion channel is a gated pore that lets specific ions cross the membrane. Note the difference from a ligand-gated channel: here the channel may open in response to voltage, not a ligand, and a drug acts as an outsider that plugs or steadies it. Calcium-channel blockers relax blood vessels exactly this way — by limiting how much calcium can flood in.
A membrane transporter is a pump or shuttle that ferries molecules across the membrane. Stall the shuttle and the molecule piles up where it was being carried from. The best-known example is the reuptake inhibitor: an SSRI antidepressant blocks the transporter that vacuums serotonin back out of the synapse, so serotonin lingers longer. A proton-pump inhibitor jams the pump that secretes stomach acid.
Subtypes: the fine-grained address
Even a single receptor name usually hides several closely related versions, called receptor subtypes. The body's adrenaline receptors split into alpha and beta types, and beta splits again into beta-1, mostly in the heart, and beta-2, mostly in the lungs. They respond to the same natural hormone but differ just enough in shape that a clever drug can tell them apart.
This is the whole point of selectivity. A drug aimed mostly at the beta-adrenoceptor subtype beta-1 can slow a racing heart while largely leaving the lung's beta-2 alone — a real advantage for someone who also has asthma. Selectivity is never perfect, and it fades at high doses, but subtypes are the reason we can steer an effect to one organ rather than the whole body.