Nervous And Hormonal Control Of Vascular Tone

Question 1

What are the two types of vascular control

Answer 1

Vascular control can be local or extrinsic and can vary between arteries and veins.

Question 2

How are arteries and veins controlled - factors

Answer 2

Both arteries and
veins are locally controlled by paracrine and autoregulation agents (nitric oxide, endothelin, ions)
and physical factors (temperature, pH and stress).

Question 3

How are arteries and veins controlled extrinsically

Answer 3

Extrinsically, both arteries and veins are controlled
by sympathetic innervation and external hormones (adrenaline, angiotensin II, vasopressin and atrial
natriuretic peptide).

Question 4

How are resistant vessels controlled - local and extrinsic

Answer 4

Only the resistant vessels, arterioles are controlled locally by myogenic response
and extrinsically by parasympathetic, sympathetic and sensory vasodilator nerves

Question 5

What are the intrinsic controls and what so they regulate

Answer 5

Intrinsic controls in general regulate local blood flow to particular organs.

Question 6

What is extrinsic control used to regulate

Answer 6

Extrinsic control is used to

mainly regulate blood pressure.

Question 7

What does nerve innervation action do to the blood

Answer 7

They may also however selectively alter blood flow to organs
according to need (e.g. exercise and thermoregulation). This is done through nerves innervating the
organs in question that originate from the brain.

Question 8

There are various nerves and hormones that cause
vasoconstriction and vasodilation.
What Hormone is responsible for vasoconstriction

Answer 8

Noradrenaline is a vasoconstrictor released from nerves whilst
acetylcholine and nitric oxide are vasodilators released from nerves. Adrenaline, angiotensin II and
vasopressin are hormonal vasoconstrictors

Question 9

What hormone is responsible for vasodilation - one

Answer 9

whilst anti-natriuretic peptide (ANP) is a hormonal

vasodilator.

Question 10

What is the most important extrinsic control

Answer 10

The sympathetic vasoconstrictor system is the most widespread and important extrinsic control. This
system is responsible for tone and the vasoconstriction of mostly arterioles (arteries to a lesser
extent)

Question 11

How often is the vasoconstriction mechanism used

Answer 11

It is fired around once a second as a pulse that sends noradrenaline to the target vessels and
makes them vasoconstrict.

Question 12

What other molecules produces vasodilation

Answer 12

There is also a background production of nitric oxide that vasodilates
these blood vessels.

Question 13

From both hormonal mechanisms what does this suggest about the vessels

Answer 13

These vessels are therefore under antagonistic control from these two systems.

Question 14

What is the advantage if the vessels having two mechanisms

Answer 14

The advantage of this is that the target vessels can both be constricted or dilated.

Question 15

What part of the brain stem receives info from the caudal ventrolateral medulla.

Answer 15

The rostral ventral lateral medulla
(RVLM) in the brainstem receives information from the caudal ventrolateral medulla (CVLM). These
two areas of the brain integrate information for the sympathetic nervous system.

Question 16

What happens when the RVLM receives info from cvlm

Answer 16

From there, an

axon moves signals to the spinal cord at the intermediolateral cell column (IML).

Question 17

Describe the IML - where do these nerves reach

Answer 17

The IML contains
pre-ganglionic sympathetic neurones that leave the spine from T1 to L2. These neurones reach the
paravertebral column, the location of most sympathetic ganglia.

Question 18

What happens to the post ganglionic neurones

Answer 18

The post-ganglionic neurones leave
the ganglia and go onto innervate many targets including the heart (beta-1 receptors), as well as
arterioles (alpha-1 receptors).

Question 19

How is blood pressure effected - multi step

Answer 19

Blood pressure can be affected by sending a nervous signal down this
type of neurone. The neurone that innervates the adrenal gland causes the release of adrenaline into
the bloodstream. Adrenaline can have the effect of causing constriction when interacting with alpha-
1 receptors, and dilation when interacting with beta-2 receptors.
The sympathetic neurones arrive from the spinal cord and innervate the smooth muscle of arterioles.
In the smooth muscle, the neurones form varicosities. When an action potential reaches a varicosity,
it is stimulated to open voltage-gated calcium channels. This causes the release of noradrenaline
stored in vesicles, from the varicosity. Some of the noradrenaline binds to alpha-2 receptors, which
are negative feedback receptors that reduce the effect of noradrenaline. The noradrenaline then
binds to alpha-1 receptors located in the smooth muscle. If the noradrenaline binds to beta-2
receptors (in some tissues), this causes relaxation. Adrenaline released by the adrenal gland can also
bind to these receptors. The noradrenaline is then taken up again where it is recycled or broken
down. There are also other receptors on the varicosity.

Question 20

What chemicals inhibit the release of noradrenaline

Answer 20

Chemicals like adenosine, potassium, PGE1,
histamine and serotonin inhibit the release of noradrenaline from its vesicles and this causes
vasodilation.

Question 21

What is Angiotensin 2

Answer 21

Angiotensin II is a hormone produced in response to change in blood pressure by the
kidneys.

Question 22

What happens when Angiotension II binds to a receptor

Answer 22

When it binds to its receptor in the varicosity, it increases the release of noradrenaline and
therefore cause vasoconstriction.

Question 23

What activation of what receptor causes vasoconstriction

Answer 23

The sympathetic nerves innervate almost all the arterioles,

arteries, venules and veins in the body. Activation of the alpha-1 receptors causes vasoconstriction.

Question 24

What is used to treat hypertension

Answer 24

There is vascular tone involved such that the vasoconstriction can be turned up and down. This
property is utilised to treat hypertension that is decreased when vasodilation occurs (e.g. calcium
channel blockers).

Question 25

What is the main role of the sympathetic nerves

Answer 25

The main roles of these nerves allows for the control of TPR and therefore blood
flow. It also allows for the distribution of blood efficiently according to certain situations (exercise,
digestion, etc).

Question 26

What does pre capillary constriction lead to

Answer 26

Pre-capillary constriction leads to decrease in pressure downstream of the arteriole
and therefore increased absorption of interstitial fluid in the capillaries.

Question 27

How can venous volume be controlled

Answer 27

Venous blood volume can

also be controlled through sympathetic innervation.

Question 28

What are the different nerves that vasodilation and vasoconstrict

Answer 28

These nerves can be
parasympathetic vasodilator nerves, sympathetic vasodilator nerves (a few) and sensory vasodilator
fibres.

Question 29

What does the parasympathetic nerve innervate

Answer 29

The parasympathetic vasodilator nerves innervate the salivary glands, releasing acetylcholine
and vasoactive intestinal peptide (VIP). This increases the blood flow to the salivary glands. There is
also innervation to the pancreas and intestinal mucosa (VIP). In both these examples, the nerves
innervate the endothelium to stimulate the synthesis of NO that causes vasodilation when in contact
with the smooth muscle of blood vessels.

Question 30

What does innervation of blood vessels of male genital cause

Answer 30

Innervation to blood vessels of the male genitalia causes

production of NO that produces cGMP that leads to vasodilation.

Question 31

How does viagra work

Answer 31

Viagra works by inhibiting the

breakdown of cGMP. The sudomotor fibres of the skin are innervated by sympathetic nerves.

Question 32

What do the sudomotor fibres do

Answer 32

The
sudomotor fibres control sweating and the nerves innervating them release Ach and VIP and also
cause the synthesis of NO for vasodilation. This increases the blood flow that causes more sweat and
allows for greater heat loss via the skin.

Question 33

What controls the action of sweating

Answer 33

This action is not only controlled by the centres of the
brainstem, but also emotional centres in the brain. These have some control over the sudomotor
fibres of the head, face, upper chest and are also involved in blushing.

Question 34

What Happens when nociceptive C fibres are stimulated

Answer 34

Another type of nerve involved in vasodilation is the sensory (nociceptive C fibres) vasodilator fibres
that when stimulated by trauma, initiate two responses. They release a substance called substance P
(or calcitonin gene-related peptide or CGRP). Substance P acts on mast cells to release granules
including histamine. Substance P also acts on the endothelium and vascular smooth muscle of the
blood vessels and cause vasodilation.

Question 35

Name the hormones in circulation which effect vasoconstriction and dilation

Answer 35

There are a few hormones that are in circulation that each cause vasoconstriction or vasodilation.
Adrenaline, angiotensin II and vasopressin (anti-diuretic hormone or ADH) are all vasoconstrictors
whilst atrial natriuretic peptide (ANP) is a vasodilator. Other hormones include insulin, oestrogen and
relaxin that also effect vasculature.

Question 36

Where is adrenaline released ——-> impulse

Answer 36

Adrenaline is released from the adrenal medulla in response to a nervous impulse. This impulse
releases acetylcholine that interacts with nicotinic AChRs to stimulate adrenaline release.

Question 37

When is adrenaline released

Answer 37

Adrenaline
is released during exercise, flight-fight-fear response, hypotension (baroreceptor reflex that detects a
drop in blood pressure) and hypoglycaemia (mobilises glucose from glycogen stores).

Question 38

What are mainly the effects of adrenaline

Answer 38

The effects of
adrenaline are mainly metabolic and CVS related. As mentioned above, it has a role in glucose
mobilisation (glycogenolysis and fat lipolysis). Adrenaline also stimulates heart rate and contractility
during normal exercise. The vasodilation of coronary and skeletal muscle arteries as well as the
vasoconstriction of other arteries to divert more blood to main tissues involves adrenaline.

Adrenaline and noradrenaline can have different effects on tissues depending on the receptor it
binds to.

Question 39

What happens to most tissues in response to noradrenaline and adrenaline

Answer 39

In most tissues (GI tract, skin, etc), both adrenaline and noradrenaline cause
vasoconstriction (due to alpha-1 receptors). With skeletal muscle and coronary circulation,
adrenaline causes vasodilation whilst noradrenaline causes vasoconstriction.

Question 40

What receptor does adrenaline have a higher affinity to

Answer 40

The reason for this is
because adrenaline has a higher affinity to beta-2 receptors than alpha-1 receptors whilst the
opposite is true with noradrenaline.

Question 41

What happens when adrenaline binds to a1 and b2

Answer 41

Adrenaline binding to beta-2 receptors causes vasodilation
whilst noradrenaline binding to alpha-1 receptors causes vasoconstriction. In this situation,
noradrenaline has the effect of increasing total peripheral resistance that has the effect of increasing
blood pressure. This stimulates the baroreceptors to decrease heart rate and therefore reduce
cardiac output.

Question 42

What is the effect of adrenaline when heart rate is decreased

Answer 42

The effect of adrenaline however is that total peripheral resistance is decreased.

Question 43

What is the action of adrenaline with beta 1

Answer 43

Adrenaline also acts on beta-1 receptors so it will increase heart rate and therefore increasing cardiac
output. The overall effect on blood pressure is not huge as whilst TPR decreases, cardiac output
increases to compensate.

Question 44

Why is noradrenaline a useful way of increasing blood pressure

Answer 44

Noradrenaline is a useful way of increasing blood pressure without
increasing heart rate (e.g. in sepsis).
Angiotensin II is released as part of the renin-angiotensin-aldosterone-system (RAAS).

Question 45

How does the kidney effect blood flow

Answer 45

There are
detectors in the kidney that measure blood pressure and osmotic potential (high osmotic potential increase blood volume and vice versa). A low blood pressure and/or low sodium levels triggers the
kidney to produce renin.

Question 46

What is the action of renin

Answer 46

Renin cleaves off 10 amino acids from angiotensinogen (precursor
synthesised in the liver that is 435 amino acids long) in a proteolysis reaction to produce angiotensin
I (decapeptide).

Question 47

What is the action of angiotensin 1

Answer 47

Angiotensin I is released in circulation and when it reaches the lungs in the vascular
endothelium, it interacts with the angiotensin converting enzyme (ACE).

Question 48

What is the action of ACE

Answer 48

ACE cleaves off 2 more

amino acids from angiotensin I to produce angiotensin II (octapeptide).

Question 49

What is the action of angiotensin 2

Answer 49

• Angiotensin II circulates
around the body causing vasoconstriction. It also has effects on the brain increasing the thirst
sensation as well as the sympathetic tone on blood vessels (increases blood pressure).
• Angiotensin II also acts on the adrenal gland above the kidney to produce aldosterone. Aldosterone is a steroid that
causes the retention of more sodium from the kidneys that has the effect of increasing NaCl levels in
the blood that increases blood volume.

Question 50

What happens when nacl is increased in the blood

Answer 50

This also has the effect of increasing blood pressure.

Question 51

What is vasopressin

Answer 51

Vasopressin is the antidiuretic hormone (ADH) that is released from the posterior pituitary gland.

Question 52

What is the function of atria stretch receptors

Answer 52

The
atria of the heart have atrial stretch receptors that measure the stretch of the walls of the atria as
well as the osmolarity of the blood. They send signals to the nucleus tractus solitarius (NTS) in the
medulla of the brainstem.

Question 53

What do NTS do

Answer 53

The NTS sends an inhibitory signal to the caudal ventrolateral medulla
(CVLM) to stop producing signals for the hypothalamus to release ADH.

Question 54

What does ADH cause

Answer 54

ADH causes vasoconstriction
as well as an increase in the reabsorption of water in the kidneys which both these increasing blood
pressure.

Question 55

What do atrial receptor and baroreceptors do - inhibit release of

Answer 55

This means the signals from the atrial receptors as well as the arterial baroreceptors inhibit
the release of ADH when the heart and blood vessels are stretched due to high blood pressure and
water potential.

Atrial receptors are low pressure baroreceptors - detects increase in vol and pressure

Question 56

What happens during dehydration or heamorrage

Answer 56

During dehydration or haemorrhage, the NTS inhibition mechanism is switched off
and CVLM stimulates the release of ADH from the hypothalamus by sending signals to the
magnocellular neurons in the supraoptic nucleus (SON) and the paraventricular nucleus (PVN).

Question 57

What is ANP and the function

Answer 57

The final hormone to discuss is the vasodilator atrial natriuretic peptide (ANP). It is released by atrial
myocytes and acts at specific receptors (ANP receptors) on smooth muscle causing vasodilation.

Question 58

What stimulates the release of ANP

Answer 58

It’s release is stimulated by increase in filling pressures that stimulate stretch receptors to release ANP.
The ANP acts at ANP receptors on vascular smooth muscle increasing cGMP pathway (e.g. the
production of nitric oxide) that opposes the action of noradrenaline, RAAS and ADH. This dilation is
especially present in the renal afferent arterioles that increases glomerulus filtration rate (GFR). This
increases the excretion of sodium and water and therefore blood volume is decreased.