The ANS Flashcards
What is the autonomic nervous system?
The autonomic nervous system is the involuntary part of the peripheral nervous system. The ANS consists of 3 divisions:
Sympathetic=‘fear, fight and flight’ parasympathetic= ‘resting and digesting’
The ENS is intrinsic to the GI tract
The sympathetic and parasympathetic link the CNS to the periphery
How is the anatomy of the ANS different to the somatic nervous system?
The anatomy of the ANS is different to that of the somatic nervous system
In the somatic nervous system, 1 neurone connects the CNS to the periphery (e.g. skeletal muscle)
In the ANS, hay 2 neurones in series – a preganglionic fibre and a postganglionic fibre
Describe the Anatomy of the Sympathetic and parasympathetic Nervous System
The sympathetic nervous system has a thoracolumbar outflow – the sympathetic preganglionic fibres arise from the spinal cord between T1 and L2
The parasympathetic nervous system has a craniosacral outflow – the preganglionic fibres arise from cranial nerves III, VII, IX and X, as well as from S2-S4
Describe chemical transmission in the ANS
The main neurotransmitters in the ANS= ACh and NA
All preganglionic fibres release ACh, which acts at ganglionic nicotinic receptors
Parasympathetic short postganglionic fibres release ACh that acts at muscarinic receptors
Exception: corpus cavernosum, where NO is released
Sympathetic long postganglionic fibres release NA that acts at adrenergic receptors
Exception: sweat glands, where ACh is released to act a muscarinic receptor
What are general rules of autonomic innervation?
The sympathetic and parasympathetic nerves systems usually produce opposing effects in the same organ (e.g. in the heart)
Sometimes, the 2 systems can produce the same effect in an organ. Eg at the salivary glands, parasympathetic stimulation produces a watery secretion, but sympathetic stimulation produces a thick, mucus rich secretion
Relate afferent and efferent fibres to the baroreceptor reflex
Hay afferent and efferent pathway in the ANS:
A stimulus activates a receptor
The receptor triggers action potentials in an afferent fibre which carries info to the CNS
In the CNS, the sensory, afferent info is processed
The CNS sends motor information back to the periphery via autonomic efferent fibres
Eg: high BP is detected by arterial baroreceptors and relayed to the CNS. The CNS then reduces sympathetic stimulation and increases parasympathetic stimulation of the heart and vsmcs – this reduces BP
Describe the structure of the sympathetic ANS
Danger signals are sent to the hypothalamus.
The hypothalamus stimulates the rostral ventrolateral medulla (RVLM).
The RVLM stimulates excitatory presympathetic fibres, which stimulate the nerve roots between T1 and L2
These nerve roots send efferent impulses to the peripheral organs via short pre and long postganglionic fibres
Postganglionic fibres release NA at adrenergic receptors on the target organs
How does the ANS stimulate adrenaline release?
1 preganglionic fibre releases ACh at the adrenal medulla, stimulating the adrenaline release into circulation.
Outline sympathetic control of the heart
NA and adrenaline act at b1-adrenoceptors to ⇡ CO: These receptors are found in the SAN, conduction system and muscle cells.
Sino-atrial node: Increases Hz of pacemaker potentials which ⇡ HR (+ve chronotropic effect)
Conduction system: ⇡ rate of impulses through atria to ventricles maintains the balance between HR and contractions (dromotropic effect)
Muscle cells : ⇡ force of contraction of atria and ventricles which ⇡ stroke volume (Inotropic effect)
Overall, hay increased SV and HR, and hence CO
Outline parasympathetic control of the heart
Stimulation of the vagus nerve (CNX) causes EACh release at M2 receptors in the SAN
This reduces pacemaker potential frequency –a negative chronotropic effect
It also decreases conduction rate from the atria to the ventricles across the AVN – a negative dromotropic effect
Since HR decreases, CO will decrease as well
Does the parasympathetic nervous system innervate ventricles or blood vessels?
Remember there is no parasympathetic innervation to the ventricles or blood vessels. So contractility and TPR remain unchanged, BP will not change much
ONLY exception: blood vessels in the corpus cavernosum dilate in response to NO release from parasympathetic nerves. This makes them engorged with blood (erection)
Remember this by Point and Shoot: erections are mediated by Parasymp, ejaculation is Symp
Describe sympathetic control of blood vessels
NA and adrenaline act at a1-adrenoceptors
Vasoconstriction causes ⇡ TPR + diverts blood flow to needed areas
Venoconstriction ⇡ return of blood to heart, which ⇡ SV and so CO (Starling’s law)
Overall, BP and drive of blood flow increases in response to sympathetic stimulation
NA and adrenaline also act at b-1 receptors in the coronary arteries and b-2 receptors in skeletal vessels to cause vasodilation. This ⇡ blood flow to the heart and skeletal muscle
How does the sympathetic ns affect the kidneys?
NA and adrenaline act at b-1 receptors in the kidney to stimulate renin secretion
Renin produces angiotensin I. ACE produces angiotensin II. Angiotensin II acts on VSMCs, causing vasoconstriction.
It also stimulates aldosterone secretion at the adrenal cortex. Aldosterone ⇡ Na retention. This causes more water to follow via osmosis, ⇡ blood volume and therefore CO (via Starling’s law)
How does the sympathetic ns affect metabolism?
In liver/skeletal muscle: a/b-adrenoceptor stimulation causes glycogenolysis and promotes glucose synthesis (gluconeogensis)
Pancreas: stimulation of a/β-adrenoceptors decreases insulin release from beta-cells. Insulin thus can’t inhibit glycogenolysis.
⇡ glucagon from alpha-cells ⇡ glycogenolysis. Blood glucose levels thus increase
Adipose tissue: stimulation of β3-adrenoceptors ⇡ lipolysis to form fatty acids + glycerol. These enter Krebs/glycolysis and increase ATP production
How does the parasympathetic ns affect the GI tract?
In the gut, parasympathetic input increases motility by speeding up the peristaltic wave that propels intestinal contents aborally
This involves the action of ACh from the vagus nerve at M3 receptors, which stimulates contraction of the muscle
Inhibitory NO and VIP also cause relaxation ahead of the bolus