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ANS & Heart
The structures and functions of the sympathetic and parasympathetic systems on the heart
differ in various ways. Presympathetic fibres originate in the brainstem, synapsing with
preganglionic fibres in T1-5 spinal cord segments bilaterally. Each preganglionic fibre
synapses with a postganglionic fibre located in the stellate ganglion of the sympathetic
chain. These fibres innervate the ventricles, the SAN and the AVN in the heart. In the
parasympathetic system, preganglionic fibres of the vagus nerve synapse with
postganglionic fibres located in the heart tissue. The postganglionic fibres only innervate
the SAN and AVN.
Sympathetic outflow to the heart causes positive chronotropy, ionotropy,
lusotropy and dromotropy (increased AVN conduction). As a result there is slow onset
tachycardia, an increased gradient and size of AP and an increased if current. The
parasympathetic system induces the opposite effects; however, the two systems do not act
symmetrically on the heart. While parasympathetic outflow reduces the if current by
causing MDP to be more negative (thus requiring the current more time to reach
threshold) the sympathetic system does not affect MDP. Parasympathetic stimulation also
induces hyperpolarisation and bradycardia.
Heart rate is determined by the duration of pacemaker potential decay i.e the time
taken for the potential to become less negative due to Na and Ca influx and inhibition of
IK. The duration of this also determines the duration of diastole. Sympathetic outflow
decreases the pacemaker potential decay via the following mechanism: NE and E activate
beta receptors coupled to Gs which activates AC and increases cAMP elvels in the ell.
CAMP activates PKC which phosphorylates effector proteins, resulting in an increased if
current rate and in L-type Ca channel activity. As a result, the rate of depolarization at
phase O increases and there is a positive chronotropic effect. The parasympathetic system
increases the pacemaker potential decay via two mechanisms. ACh directly activates
Ikach channels (normally background IK inactive) resulting in an influx of K ions,
hyperpolarizing the cell. ACh also binds M2 receptors that are coupled to Gi and inhibit
AC. Resulting cAMP levels are lowered which decrease L-type Ca channel activity, the if
current and result in negative chronotropy. Sympathetic outflow (in the form of
isoprenaline, NE or E) causes a positive ionotropic effect on ventricular CMCs. This is
done by increasing intracellular Ca levels. Increasing SERCA activity also causes
positive lusotropy as more Ca is taken up into the SR. SERCA is also controlled by the
RyR channel on SR membrane that is phosphorylated by PKA, increasing its Ca pump
activity.
Presynaptic inhibition of both autonomic nervous systems ensures their reciprocal
activity. Figure 3 shows reciprocal inhibition. At rest HR is lowered from 100 bpm to
70bpm by vagal tone. During exercise sympathetic activity increases and
parasympathetic activity decreases.
ANS structure
The peripheral nervous system is the conduit between CNS and the external/internal
environment. ANS consists of preganglionic neurons that originate in the CNS and
synapse onto postganglionic nerves on ganglions, which then innervate effector organs.
These connections can be inhibitory or excitatory via nerve endings and varicosities but
there are no motor end plates or NMJs like in the somatic NS. ANS action is spontaneous
and involuntary and the two systems antagonise each other but remain in balance. Figure
1 – structure of NS. Exception to the model: skeletal muscle of the diaphragm/intercostals
innervated by autonomic control. Sympathetic preganglionic fibres originate in T1-12 and
L1-3 regions of the SC (in lateral horn), are short, myelinated and synapse with and
release ACh onto long (unmyelinated) postganglionic fibres at the paravertebral ganglia
which then release NE onto effector organs. Long parasympathetic preganglionic fibres
form the vagus and pelvic nerves that originate in the brainstem, synapse with
postganglionic fibres on fewer effector organs, releasing ACh onto them. The
postganglionic fibres also release ACh and mediate parasympathetic effects. Major
effects of the sympathetic system are: increased adrenaline release from adrenal medulla;
increased renin release; ejaculation in males; arteriolal vasoconstriction via alpha1/2
activation; minor dilation of skin and skeletal muscle vessels via beta activation and
coronary dilation. Major parasympathetic effects are: increased GI motility; decreased
sphincter tone; penile vasodilation leading to erection; skin vasodilation; increased
glandular and GI secretion and coronary contraction. While blood flow is mostly
increased by the ‘rest and digest’ parasympathetic system it is mostly decreased by the
‘fight or flight’ sympathetic system. In the brainstem (CNS) there are various control
centres that mediate systemic homeostasis. The hypothalamus is involved in
thermoregulation and osmoregulation; the respiratory centre and cardio inhibitory centre
control pCO2-dependent ventilation rate and decrease HR respectively. The
cardioacceleratory centre in the pons causes an increase in HR. The pneumotaxic centre,
also in the brainstem, is involved in rhythmic inspiration inhibition to control amount of
air inhaled. There is NANC transmission in the parasympathetic postganglionic fibre, off
which comes a NANC fibre that releases VIP onto blood vessels. This hormone
potentiates ACh action, causing vasodilation in arterioles and coronary arteries.
In extreme conditions – fight or flight, balanced at rest with adjustment for
exercise or temp change.