Beta-blockers: turning down the sympathetic drive
A beta-blocker (the '-olol' drugs, e.g. metoprolol, bisoprolol) sits on beta-adrenoceptors and blocks adrenaline and noradrenaline from reaching them. In the heart, β1 receptors drive rate and force, so blocking them slows the heart and lowers cardiac output. They also cut the kidney's renin release, dialling down the RAAS too — a tidy double effect.
Calcium-channel blockers: two families, two jobs
Muscle cells need calcium influx to contract. A calcium-channel blocker shuts the L-type calcium channel, so muscle relaxes. The split matters: dihydropyridines (the '-dipine' drugs, e.g. amlodipine) act mostly on vessel walls — strong vasodilators, little effect on heart rate. Non-dihydropyridines (verapamil, diltiazem) act more on the heart itself, slowing rate and conduction.
Diuretics: emptying the tank through the kidney
A diuretic tells the kidney to excrete more salt, and water follows the salt out — shrinking blood volume and BP. A thiazide diuretic (e.g. hydrochlorothiazide) acts on the distal tubule; it is mild, cheap, and a first-line antihypertensive. A loop diuretic (e.g. furosemide) acts on the loop of Henle; it is far more powerful and the go-to for clearing fluid overload in heart failure.
Their main downside is electrolyte loss. Thiazides and loop diuretics waste potassium, which can trigger arrhythmias — a side effect you watch with blood tests. (Note the contrast with RAAS blockers and spironolactone, which raise potassium; pairing the two is a deliberate way to balance the books.)