Autonomic Control Of The Cardiovascular System
The autonomic nervous system (ANS) comprises a system of efferent
nerves that regulate the involuntary functioning of most organs, including
the heart and vasculature. The cardiovascular effects of the ANS are deployed
for two purposes.
First, the ANS provides the effector arm of the cardiovascular reflexes,
which respond mainly to activation of receptors in the cardiovascular system
(see Chapter 27). They are designed to maintain an appropriate blood
pressure, and have a crucial role in homeostatic adjustments to postural
changes (see Chapter 22), haemorrhage (see Chapter 31) and changes
in blood gases. The autonomic circulation is able to override local
vascular control mechanisms in order to serve the needs of the body as a whole.
Second, ANS function is also regulated by signals initiated within the
brain as it reacts to environmental stimuli or emotional stress.
The brain can selectively modify or override the cardiovascular reflexes,
producing specific patterns of cardiovascular adjustments, which are sometimes
coupled with behavioural responses. Complex responses of this type are involved
in exercise (see Chapter 30), thermoregulation (see Chapter 25),
the ‘fight or flight’ (defence) response and ‘playing dead’.
The ANS is divided into sympathetic and parasympathetic branches.
The nervous pathways of both branches of the ANS consist of two sets of neurones
arranged in series. Preganglionic neurones originate in the central
nervous system and terminate in peripheral ganglia, where they synapse
with postganglionic neurones innervating the target organs.
Sympathetic preganglionic neurones originate in the intermediolateral (IML)
columns of the spinal cord. These neurones exit the spinal cord through ventral
roots of segments T1–L2, and synapse with the
postganglionic fibres in either paravertebral or prevertebral ganglia.
The paravertebral ganglia are arranged in two sympathetic chains, one of which
is shown in Figure 28. These are
located on either side of the spinal cord, and usually contain 22 or 23
ganglia. The prevertebral ganglia, shown to the left of the sympathetic chain,
are diffuse structures that form part of the visceral autonomic plexuses of the
abdomen and pelvis. The ganglionic neurotransmitter is acetylcholine,
and it activates postganglionic nicotinic cholinergic receptors.
The postganglionic fibres terminate in the effector organs, where they
release noradrenaline. Preganglionic sympathetic fibres also control the
adrenal medulla, which releases adrenaline and noradrenaline into the blood. Under
physiological conditions, the effect of neuronal noradrenaline release is more
important than that of adrenaline and noradrenaline released by the adrenal
medulla.
Adrenaline and noradrenaline are catecholamines, and activate adrenergic
receptors in the effector organs. These receptors are g-protein-linked and
exist as three types.
1 α1-receptors
are linked to Gq and have subtypes α1A, α1B
and α1D. Adrenaline and
noradrenaline activate α1-receptors with similar potencies.
2 α2-receptors
are linked to Gi/o and have subtypes α2A, α2B
and α2C. Adrenaline
activates α2-receptors more potently than does noradrenaline.
3 β-receptors
are linked to Gs and have subtypes β1, β2
and β3.
Noradrenaline is more potent than adrenaline at β1- and β3-
receptors, while adrenaline is more potent at β2-receptors.
Effects On The Heart
Catecholamines acting via cardiac β1-receptors have
positive inotropic and chronotropic effects via mechanisms described in Chapters
12 and 13. At rest, cardiac sympathetic nerves exert a tonic accelerating
influence on the sinoatrial node, which is, however, overshadowed in younger
people by the opposite and dominant effect of parasympathetic vagal tone. Vagal
tone decreases progressively with age, causing a rise in the resting heart rate
as the sympathetic influence becomes more dominant.
Effects on the vasculature
At rest, vascular sympathetic nerves fire impulses at a rate of 1–2
impulses/s, thereby tonically vasoconstricting the arteries, arterioles and
veins. Increasing activation of the sympathetic system causes further
vasoconstriction. Vasoconstriction is mediated mainly by α1-receptors
on the vascular smooth muscle cells. The arterial system, particularly the
arterioles, is more densely inner- vated by the sympathetic system than is the
venous system. Sympathetic vasoconstriction is particularly marked in the splanchnic,
renal, cutaneous and skeletal muscle vascular beds.
The vasculature also contains both β1- and β2-receptors,
which when stimulated exert a vasodilating influence, especially in the skeletal
and coronary circulations. These may have a limited role in dilating
these vascular beds in response to adrenaline release, for example during
mental stress. In some species, sympathetic cholinergic fibres innervate
skeletal muscle blood vessels and cause vasodilatation during the defence
reaction. A similar but minor role for such nerves in humans has been proposed,
but is unproven. It is a common fallacy that the sympathetic nerves are always
activated en masse. In reality, changes in sympathetic vasoconstrictor
activity can be limited to certain regions (e.g. to the skin during
thermoregulation). Similarly, a sympathetically mediated tachycardia occurs
with no change in inotropy or vascular resistance during the Bainbridge reflex (see Chapter 27).
The Parasympathetic System
The parasympathetic preganglionic neurones involved in regulating the
heart have their cell bodies in the nucleus ambiguus and the dorsal
motor nucleus of the medulla. Their axons run in the vagus nerve
(cranial nerve X) and release acetylcholine onto nicotinic receptors on short
postganglionic neurones originating in the cardiac plexus. These innervate the sinoatrial
node (SAN), the atrioventricular node (AVN) and the atria.
Effects On The Heart
Basal acetylcholine release by vagal nerve terminals acts on muscarinic
receptors to slow the discharge of the SAN. Increased vagal tone further
decreases the heart rate and the speed of impulse conduction through the AVN
and also decreases the force of atrial contraction when activated.
Effects On The Vasculature
Although vagal slowing of the heart can decrease the blood pressure by
lowering cardiac output, the parasympathetic system has no effect on total
peripheral resistance, because it innervates only a limited number of vascular
beds. In particular, activation of parasympathetic fibres in the pelvic nerve
causes erection by vasodilating arterioles in the erectile tissue of the
genitalia. Para-sympathetic nerves also cause vasodilatation in the pancreas
and salivary glands.
