Nervous And Hormonal Control Of Vascular Tone Flashcards
What are the two types of vascular control
Vascular control can be local or extrinsic and can vary between arteries and veins.
How are arteries and veins controlled - factors
Both arteries and
veins are locally controlled by paracrine and autoregulation agents (nitric oxide, endothelin, ions)
and physical factors (temperature, pH and stress).
How are arteries and veins controlled extrinsically
Extrinsically, both arteries and veins are controlled
by sympathetic innervation and external hormones (adrenaline, angiotensin II, vasopressin and atrial
natriuretic peptide).
How are resistant vessels controlled - local and extrinsic
Only the resistant vessels, arterioles are controlled locally by myogenic response
and extrinsically by parasympathetic, sympathetic and sensory vasodilator nerves
What are the intrinsic controls and what so they regulate
Intrinsic controls in general regulate local blood flow to particular organs.
What is extrinsic control used to regulate
Extrinsic control is used to
mainly regulate blood pressure.
What does nerve innervation action do to the blood
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.
There are various nerves and hormones that cause
vasoconstriction and vasodilation.
What Hormone is responsible for vasoconstriction
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
What hormone is responsible for vasodilation - one
whilst anti-natriuretic peptide (ANP) is a hormonal
vasodilator.
What is the most important extrinsic control
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)
How often is the vasoconstriction mechanism used
It is fired around once a second as a pulse that sends noradrenaline to the target vessels and
makes them vasoconstrict.
What other molecules produces vasodilation
There is also a background production of nitric oxide that vasodilates
these blood vessels.
From both hormonal mechanisms what does this suggest about the vessels
These vessels are therefore under antagonistic control from these two systems.
What is the advantage if the vessels having two mechanisms
The advantage of this is that the target vessels can both be constricted or dilated.
What part of the brain stem receives info from the caudal ventrolateral medulla.
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.
What happens when the RVLM receives info from cvlm
From there, an
axon moves signals to the spinal cord at the intermediolateral cell column (IML).
Describe the IML - where do these nerves reach
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.
What happens to the post ganglionic neurones
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).
How is blood pressure effected - multi step
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.
What chemicals inhibit the release of noradrenaline
Chemicals like adenosine, potassium, PGE1,
histamine and serotonin inhibit the release of noradrenaline from its vesicles and this causes
vasodilation.
What is Angiotensin 2
Angiotensin II is a hormone produced in response to change in blood pressure by the
kidneys.
What happens when Angiotension II binds to a receptor
When it binds to its receptor in the varicosity, it increases the release of noradrenaline and
therefore cause vasoconstriction.
What activation of what receptor causes vasoconstriction
The sympathetic nerves innervate almost all the arterioles,
arteries, venules and veins in the body. Activation of the alpha-1 receptors causes vasoconstriction.
What is used to treat hypertension
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).
What is the main role of the sympathetic nerves
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).
What does pre capillary constriction lead to
Pre-capillary constriction leads to decrease in pressure downstream of the arteriole
and therefore increased absorption of interstitial fluid in the capillaries.
How can venous volume be controlled
Venous blood volume can
also be controlled through sympathetic innervation.
What are the different nerves that vasodilation and vasoconstrict
These nerves can be
parasympathetic vasodilator nerves, sympathetic vasodilator nerves (a few) and sensory vasodilator
fibres.
What does the parasympathetic nerve innervate
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.
What does innervation of blood vessels of male genital cause
Innervation to blood vessels of the male genitalia causes
production of NO that produces cGMP that leads to vasodilation.
How does viagra work
Viagra works by inhibiting the
breakdown of cGMP. The sudomotor fibres of the skin are innervated by sympathetic nerves.
What do the sudomotor fibres do
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.
What controls the action of sweating
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.
What Happens when nociceptive C fibres are stimulated
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.
Name the hormones in circulation which effect vasoconstriction and dilation
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.
Where is adrenaline released ——-> impulse
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.
When is adrenaline released
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).
What are mainly the effects of adrenaline
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.
What happens to most tissues in response to noradrenaline and adrenaline
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.
What receptor does adrenaline have a higher affinity to
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.
What happens when adrenaline binds to a1 and b2
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.
What is the effect of adrenaline when heart rate is decreased
The effect of adrenaline however is that total peripheral resistance is decreased.
What is the action of adrenaline with beta 1
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.
Why is noradrenaline a useful way of increasing blood pressure
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).
How does the kidney effect blood flow
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.
What is the action of renin
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).
What is the action of angiotensin 1
Angiotensin I is released in circulation and when it reaches the lungs in the vascular
endothelium, it interacts with the angiotensin converting enzyme (ACE).
What is the action of ACE
ACE cleaves off 2 more
amino acids from angiotensin I to produce angiotensin II (octapeptide).
What is the action of angiotensin 2
• 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.
What happens when nacl is increased in the blood
This also has the effect of increasing blood pressure.
What is vasopressin
Vasopressin is the antidiuretic hormone (ADH) that is released from the posterior pituitary gland.
What is the function of atria stretch receptors
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.
What do NTS do
The NTS sends an inhibitory signal to the caudal ventrolateral medulla
(CVLM) to stop producing signals for the hypothalamus to release ADH.
What does ADH cause
ADH causes vasoconstriction
as well as an increase in the reabsorption of water in the kidneys which both these increasing blood
pressure.
What do atrial receptor and baroreceptors do - inhibit release of
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
What happens during dehydration or heamorrage
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).
What is ANP and the function
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.
What stimulates the release of ANP
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.
