The Lab / Core medicine / Lesson 6
Your organs are wired to an accelerator and a brake. Follow one signal from nerve to organ, across a gap and into a receptor, then see how seven kinds of drugs press, release or jam those pedals.
Educational, not for clinical use
Build the signal
Some nerves work without you ever thinking about them. They make up the autonomic nervous system: wiring from the brain and spinal cord to the organs that keep you alive, such as the heart, blood vessels, lungs, eyes and gut.
Build the signal
The sympathetic branch (red) is the accelerator: it readies you for “fight or flight”. The parasympathetic branch (green) is the brake: it runs “rest and digest”. Most organs get both, and both work all the time, a little more or less.
Build the signal
A nerve ending stops just short of the organ’s cells. That tiny gap is the synapse. To cross it, the nerve releases a neurotransmitter: a chemical messenger that drifts over the gap in a split second and passes the signal on.
Build the signal
Parasympathetic nerves release acetylcholine (green dots). It works only where it can dock on a receptor: a site on the cell shaped to fit one messenger, like a lock for a key. On organs, its receptors are called muscarinic receptors.
Build the signal
An enzyme is a protein that makes one chemical change happen. Cholinesterase, waiting in the gap, chops acetylcholine apart within moments. So the brake acts only while the nerve keeps firing, and lets go soon after it stops.
Build the signal
Each dot on the strip is one heartbeat, so closer dots mean a faster heart rate. At rest, acetylcholine on the heart’s muscarinic receptors holds the rate down, like a foot resting on the brake.
Build the signal
Sympathetic nerves release noradrenaline (red dots), also called norepinephrine. It docks on adrenergic receptors, which come in two main families: alpha receptors and beta receptors. Which family an organ carries decides how it answers.
Build the signal
Through beta receptors on the heart, noradrenaline does the opposite of acetylcholine: the heart beats faster, and each beat squeezes harder, shown by the new bar. More blood is pumped every minute.
Build the signal
Arterioles are the smallest arteries, ringed with muscle. Through alpha receptors, noradrenaline tightens that muscle, so they narrow. Blood is harder to push through, and blood pressure, the push of blood on artery walls, rises.
Build the signal
Sympathetic nerves also reach the adrenal glands, small glands on top of the kidneys. They answer by releasing adrenaline, a close cousin of noradrenaline, into the blood, so it reaches beta receptors even where no nerve does.
Build the signal
The pupil is the dark opening of the eye. A ring muscle with muscarinic receptors makes it smaller when acetylcholine arrives; a spoke-like muscle with alpha receptors makes it larger when noradrenaline arrives. Its size shows which branch is winning.
Build the signal
The airways are the tubes carrying air into the lungs, wrapped in muscle. Acetylcholine from parasympathetic nerves tightens it, narrowing them. Sympathetic nerves barely reach this muscle; adrenaline in the blood relaxes it through beta receptors, widening them.
Build the signal
Sensors in the arteries feel blood pressure and report to the brain. If pressure rises, the brain eases the accelerator and presses the brake, so the heart slows; if pressure falls, the reverse. This automatic answer is a reflex. Lesson 4 covers it.
Build the signal
Two nerve messengers, three receptor families. Acetylcholine on muscarinic receptors slows the heart and narrows pupil and airways; noradrenaline on alpha and beta receptors tightens arterioles and speeds the heart, while adrenaline in the blood opens airways. Key measures: heart rate and blood pressure.
What changes it
An agonist is a drug that docks on a receptor and switches it on, mimicking the messenger. Muscarinic agonists, such as pilocarpine, act like extra acetylcholine: the heart slows, the pupil and airways narrow, and the gut and glands get busier.
What changes it
An antagonist, or blocker, docks on a receptor without switching it on, so the messenger cannot get in. Muscarinic antagonists, such as atropine, release the brake: the heart speeds up, and the pupil and airways widen.
What changes it
An inhibitor is a drug that stops an enzyme working. Cholinesterase inhibitors leave acetylcholine unchopped, so it builds up in the gap and keeps docking. Every muscarinic effect grows: the heart slows, and the pupil and airways narrow.
What changes it
Alpha receptors come in subtypes; alpha-1 receptors sit on the muscle of arterioles and the pupil. Alpha-1 agonists, such as phenylephrine, switch them on: arterioles narrow and blood pressure rises, the reflex slows the heart, and the pupil widens.
What changes it
Alpha-1 blockers keep noradrenaline off alpha-1 receptors. Arteriole muscle relaxes, the arterioles widen and blood pressure falls. The reflex presses the accelerator, so the heart speeds up through beta receptors, which are still free. The pupil narrows.
What changes it
Nonselective beta agonists, such as isoproterenol, switch on every beta receptor. The heart beats faster and harder, and the airways widen. Beta receptors in some blood vessels relax them, so pressure need not rise and can even fall.
What changes it
Beta blockers keep noradrenaline off beta receptors. The heart beats slower and less forcefully, and blood pressure falls. In the airways, blocking beta receptors keeps adrenaline from relaxing the muscle, so some beta blockers can narrow the airways.
Start with Next, or use the arrow keys. Sizes and spacing are illustrative, not measurements.
Loading reference values…
Normal teaching baseline.
The blue line on each bar is an illustrative teaching model, not a patient measurement. For blood pressure, the shaded zone is the guideline’s “normal” category, which has only an upper limit, so the zone runs to the left edge of the bar. For heart rate, the dashed line is the guideline’s diagnostic threshold for sinus bradycardia: a definition, not a normal range, so nothing is shaded. Arrows appear only where the cited source gives a direction for that exact row; where a source speaks of blood pressure as a whole, the summary says so and no row arrow is shown. Real responses vary.
An illustrative teaching model of both branches. Change how hard each nerve fires, block or switch on each receptor family, slow the clean-up enzyme, or switch the pressure reflex off, and watch the organs answer. The faint dashed outlines are the normal state.
Everything is relative to a normal resting state, where every quantity equals 1. Each branch has a drive (how hard its nerves fire). Acetylcholine in the gap is the parasympathetic drive divided by how fast cholinesterase clears it. The muscarinic signal is acetylcholine plus any muscarinic agonist, times the share of muscarinic receptors left free; the alpha and beta signals are built the same way from noradrenaline. Heart rate rises with the beta signal and falls with the muscarinic signal; the heart’s squeeze strength rises with the beta signal; arteriole tightness rises with the alpha signal and eases a little with beta signals from adrenaline and any beta agonist, standing in for the beta receptors that relax some blood vessels. Blood pressure is the product of squeeze strength, arteriole tightness and the square root of heart rate. The heartbeat strip is an abstract beat counter (one dot per beat), not a heart tracing; squeeze strength has its own bar. With the reflex on, pressure above normal lowers the sympathetic drive and raises the parasympathetic drive to the heart and arterioles (and the reverse), and the model finds the steady state where the pressure the reflex feels equals the pressure produced. Pupil and airway width are the ratio of their widening signal to their narrowing muscarinic signal, at resting drive; the reflex is not applied to them. The pupil widens through alpha receptors fed by sympathetic nerves. Airway muscle has almost no sympathetic nerves, so its beta signal comes from adrenaline released into the blood by the adrenal glands, which the model ties to the sympathetic drive slider. The model treats each drug as acting on every receptor of its family; real drugs often favour one subtype (for example beta-1 in the heart, beta-2 in the airways). It leaves out the gut, glands, sweat glands, adrenaline’s own action on the heart, nicotinic receptors and anything about timing. In the Clinical values tab the relative results are scaled to illustrative numbers, as that tab explains.