Page created on November 8, 2019. Last updated on January 24, 2022 at 16:11
There are two major regulatory nervous systems in the body, the parasympathetic and the sympathetic. The heart is innervated by both systems. The two systems have mostly opposite effects.
We usually think of the parasympathetic and sympathetic systems as being either “on” or “off”, but that’s not the case. Both systems can be active anywhere from 0% to 100% of full activity.
Parasympathetic activation of the heart
The major parasympathetic nerve of the body is the tenth cranial nerve, the vagal (vagus) nerve. It is a paired nerve, so there is one on the left side and one on the right.
The vagal nerve innervates the SA node, the AV node and the atria, but not the ventricles. Parasympathetic stimulation has the following effects on the heart:
- Negative chronotropic effect – decreasing heart rate
- Negative dromotropic effect – decreased conduction velocity through AV node
- Increases the PQ interval
- Negative inotropic effect – decreased contractility
- Only in the atria!
It does not affect the inotropy of the ventricles.
Mechanism of action:
Preganglionic parasympathetic fibres (the vagal nerve) terminate on the body of postganglionic neurons in the intramural ganglia in the heart. When the vagal nerve is stimulated the preganglionic fibres will release a neurotransmitter called acetylcholine into the ganglia. Acetylcholine will bind to so-called muscarinic acetylcholine receptors on postganglionic neurons. This will stimulate the postganglionic neurons, which will release acetylcholine to stimulate muscarinic receptors in the SA node, AV node and atria.
A molecule called atropine blocks muscarinic receptors so that acetylcholine cannot bind to them. This means that atropine can block the parasympathetic activation of the heart.
Sympathetic activation of the heart
The sympathetic trunk innervates the SA node, AV node, atria and ventricles.
Sympathetic stimulation has the following effects on the heart:
- Positive chronotropic effect – increasing heart rate
- Positive dromotropic effect – increasing conduction velocity through AV node
- Positive inotropic effect – increased contractility
- In both the atria and ventricles
In rest the sympathetic nervous system is at about 30% activity, so even in rest the heart receives some sympathetic stimulation. If the sympathetic activity is reduced below this the heart rate and contractility can decrease below the normal.
Mechanism of action:
Preganglionic sympathetic fibres (the sympathetic trunk) terminate on the body of postganglionic neurons in paravertebral ganglia. When the sympathetic nervous system is stimulated the preganglionic fibres will release acetylcholine into the ganglia. Acetylcholine will bind to muscarinic acetylcholine receptors on postganglionic neurons. This will stimulate the postganglionic neurons, which will release norepinephrine into the SA node, AV node, atria and ventricles, where it will bind to so-called beta-1 adrenergic receptors.
A type of drug called beta blockers block the beta adrenergic receptors so that norepinephrine cannot bind to them. Beta blockers, like propranolol, can therefore block the sympathetic activation of the heart.