Nervous and hormonal control of vascular tone Flashcards
(24 cards)
Describe an overview of vascular control
Intrinsic control (inside the tissue itself)
Happens locally in the tissue or organ.
Makes sure each tissue gets the blood it needs.
Includes:
Myogenic response (muscle in vessel walls reacts to stretch)
Paracrine & autocrine signals (local chemical messengers)
Physical factors (like temperature, or how fast blood is moving)
Extrinsic control (from outside, like nerves or hormones)
Comes from the brain or hormones circulating in the blood.
Adjusts overall blood flow based on body needs.
Includes:
Nerves (sympathetic, parasympathetic) that can tighten or relax vessels
Hormones like adrenaline or angiotensin II that can constrict or dilate vessels
This mainly controls the total blood pressure and blood distribution.
Arteries/arterioles → control total peripheral resistance (TPR = how hard it is for blood to flow through the system).
Veins/venules → act as a reservoir holding most of the blood.
Together, intrinsic + extrinsic controls balance blood flow across the body and within local tissues.
Explain the sympathetic vasoconstrictor system
✅ 1. Brain (medulla oblongata)
Receives information and decides when to increase or decrease blood vessel tone.
✅ 2. Spinal cord (T1–L2 region)
Contains special nerve cells (preganglionic sympathetic neurons) that send signals outward.
✅ 3. Preganglionic fibres
These are the first nerve fibers that leave the spinal cord and go to the sympathetic ganglia (small relay stations).
✅ 4. Sympathetic ganglia
Here, the signal is passed to the postganglionic fibres.
✅ 5. Postganglionic fibres
These directly reach the blood vessels and release noradrenaline (norepinephrine).
What does noradrenaline do
On α1 receptors → causes constriction (narrows blood vessels, increases blood pressure).
On β1 receptors → increases heart rate (HR) and stroke volume (SV) (how much blood the heart pumps).
On β2 receptors → can cause relaxation in some vessels (like in muscles).
Explain the transmission of noradrenaline
1) An action potential moves down the axon and arrive at a varicosity.
2) Depolarisation at the varicosity activating voltage gated Ca2+ channels.
3) Ingress of calcium causes release of
neurotransmitters - mainly noradrenaline.
NA diffuses to the vascular smooth muscle cells where it binds mainly α1 – contraction; some α2 – contraction and β2 – relaxation.
4) Modulation of responses in both constriction and dilatation.
5) The noradrenaline is then taken up again and recycled or broken down.
Explain varicosity detail
Release of NA can be modulated by
Angiotensin II acting on AT1 receptor
increasing NA release.
Metabolites prevent vasoconstriction to
maintain blood flow; K+, adenosine,
histamine & serotonin etc. feed back and
inhibit NA release.
NA can also negatively feed back itself via
α2 receptors to limit its own release.
Lots of modulation occurring at the
neurotransmitter level at the varicosity.
It produces vasoconstriction and vasodilation
as required.
Explain sympathetic vasoconstrictor nerves
✅ Who controls them?
The brainstem does, especially:
Rostral ventrolateral medulla (RVLM) → main controller.
Caudal ventrolateral medulla (CVLM) and hypothalamus help regulate it.
This system gives central (brain-based) control over blood flow and blood pressure.
✅ Where do these nerves go?
They go to most small arteries (arterioles) and veins.
✅ What do they do?
They release noradrenaline (NA), which:
Activates α1-adrenoceptors on the smooth muscle around blood vessels.
This makes the muscle contract → vasoconstriction (narrowing of blood vessels).
✅ What’s special about their activity?
The system works in a tonic way — meaning it’s always lightly active (about 1 nerve signal per second), not just switched on/off.
This sets the baseline (tone) of blood vessels.
✅ Why is this medically important?
If you reduce sympathetic nerve activity, blood vessels dilate (open up), lowering blood pressure.
This is a key strategy for treating conditions like hypertension (high blood pressure).
Discuss main roles of sympathetic vasoconstrictor nerves
1) Distinct sympathetic pathways innervate different tissues:
-switching on/off vasodilation in vessels. During exercise increased sympathetic nerve stimulation to GI —-> reduces sympathetic nerve stimulation to skin
2) Control resistance arterioles:
-produces vascular tone allows vasodilation/vasoconstriction controlling TPR ——> maintains arterial BP and blood flow to brain myocardium and kidney
3) Pre capillary vasoconstriction:
-leads to downstream capillary pressure drop so increase absorption of interstitial fluid into blood plasma (to maintain blood volume)
4) Control venous blood volume:
-venoconstriction leads to decreased venous blood volume increasing venous return —-> increases stroke volume via starling’s law and so increases stroke output
Explain vasodilator nerves
Vasodilatation usually occurs when vascular tone produced by sympathetic vasoconstrictor nerves is
inhibited.
A few specialised tissues contain vasodilator nerves, as well as vasoconstrictor nerves.
Normally these have a specific function controlling a specific vascular bed rather than global functions.
A few sympathetic vasodilator nerves exist eg. Sensory (nociceptive C fibres) vasodilator fibres
Explain how specific vasodilator nerves are mainly parasympathetic
Specific vasodilator nerves are mainly parasympathetic.
Some blood vessels are innervated by parasympathetic cholinergic fibres (eg. coronary vessels). These release acetylcholine (Ach) which binds to muscarinic receptors on the smooth muscle and/or endothelium.
M3 receptors located on the vascular endothelium can coupled to the formation of nitric oxide (NO) causing vasodilation. However, ACh also can also cause contraction of
smooth muscle via M2 and M3 receptors but usually less predominant than the NO
effect.
Cerebral arteries appear to have M5 muscarinic receptors that vasodilate in response to ACh.
Give examples of parasympathetic vasodilators
Parasympathetic:
Salivary glands – release acetylcholine (Ach) vasoactive intestinal peptide (VIP)
Pancreas & intestinal mucosa – release VIP
Both these tissues need high blood flow to maintain fluid secretion.
Ach/VIP tact on endothelium o cause release of nitric oxide (NO) - vasodilatation
Male genitalia (erectile tissue) – release NO. Release of NO by parasympathetic nerves causes production of cGMP which leads to vasodilatation.
Sildenafil (Viagra) enhances this effect of NO by inhibiting the breakdown of cGMP by Phosphodiesterase-5.
give examples of sympathetic vasodilators
Skin (sudomotor fibres) release Ach, VIP
causing vasodilatation via NO associated with sweating – increased blood flow causes more sweat and also allows heat loss via skin.
Sympathetic activity vasoconstriction would only reduce blood flow, limit sweat production and limit cooling.
Emotional centres in brain have some control over these fibres, head, face, upper chest, involved in blushing.
Describe what happens when there is a trauma
1) Sensory Nerves Get Activated: There are special nerve endings called “nociceptive C fibres” that feel pain. When you get hurt, these nerves get stimulated.
2) Sending Signals and Releasing Stuff: These nerves do two main things:
They send a pain signal up to your spinal cord (shown by the “Main axon” going to the “Dorsal root ganglion”).
Near the injury, they release chemicals like “Substance P” and “calcitonin gene-related peptide (CGRP)”.
3) Mast Cells Get Chatty: Substance P makes special cells called “mast cells” release another chemical called “histamine”.
4) Blood Vessels Open Up (“Flare”): Histamine causes the tiny blood vessels in the injured area to widen. This widening is called “vasodilation” and it makes the skin look red. This flare is also partly caused by a reflex action of the sensory nerves themselves widening the blood vessels.
5) The “Lewis Triple Response”: All this leads to what’s called the “Lewis triple response,” which has three parts:
Redness: From the tiny blood vessels widening.
Flare: A wider redness due to the reflex action causing more blood vessel widening.
Wheal: Swelling caused by fluid leaking out of the blood vessels.
5) Inflammation Starts: This whole process is the beginning of “inflammation.” The increased blood flow brings more immune cells and other helpful substances to the site of the injury to help it heal and fight off any germs.
Describe different hormonal control of circulation and examples
1) Vasoconstrictors:
-adrenaline
-angiotensin II
-vasopressin
2) Vasodilators:
-atrial natruietic peptide
3) others (e.g. Insulin)
-also effects on vasculature
Explain characteristics of adrenaline (epinephrine)
Adrenaline is released from adrenal medulla – via action
of acetylcholine on nicotinic receptors during…
Exercise
Flight-Fight-Fear response (increase sympathetic drive)
Hypotension (baroreceptor reflex)
Hypoglycaemia
Main roles – metabolic and CVS effects
Glucose mobilisation (skeletal muscle glycogenolysis, fat lipolysis,
β3)
Stimulation of heart rate & contractility during normal exercise (β1)
Vasodilatation of coronary and skeletal muscle arteries (β2)
Explain the difference between Adrenaline and noradrenaline on resistance vessels
Noradrenaline’s Main Job:
It mostly uses a door called α
1 receptors.
When noradrenaline opens these α
1 doors, it usually causes the blood vessels to constrict (get narrower).
This happens in most tissues, like those in your gut. It also happens in the blood vessels of your skeletal muscles and heart (coronary arteries), which have more α
1- receptors.
Adrenaline’s Different Approaches:
-Adrenaline can use both α
1 and β receptors.
-It has a stronger preference for β
2 receptors.
-When adrenaline opens β
2 receptors it usually causes the blood vessels to dilate (widen), especially in skeletal muscle.
-However, adrenaline can also use α
1 receptors and cause constriction in some tissues.
Discuss what happens in the circulation when you are only given adrenaline through an IV
Let’s look at what happens when ONLY adrenaline is given:
Heart Rate: Goes up a lot initially.
Arterial Pressure (Blood Pressure): Goes up, then comes down a bit.
Cardiac Output (how much blood your heart pumps): Goes up significantly.
Total Peripheral Resistance (how constricted your blood vessels are): Goes down. This is because adrenaline affects β
2 receptors in skeletal muscle arterioles, causing them to widen
Discuss what happens to the circulation when only noradrenaline is given through IV
Now, let’s see what happens when ONLY noradrenaline is given:
Heart Rate: Goes down. Why? Because noradrenaline strongly increases blood pressure. This triggers a reflex (baroreceptor reflex) that slows down your heart rate to try and bring the blood pressure back down.
Arterial Pressure (Blood Pressure): Goes up a lot and stays high.
Cardiac Output: Doesn’t change much or might slightly decrease (because the heart rate slows down).
Total Peripheral Resistance: Goes up a lot. This is because noradrenaline mainly acts on α -1 receptors, causing blood vessels to constrict.
Explain the renin-angiotensin-aldosterone system (RAAS)
Low salt (Na +) levels reaching a specific part of your kidney.
Lower blood pressure sensed by cells in your kidney.
Your “fight or flight” nervous system (sympathetic activity) kicking in on your kidneys.
-When any of these happen, your kidneys release a helper enzyme called Renin
-Renin then acts on a protein floating in your blood made by the liver called Angiotensinogen and chops it up to create Angiotensin I
Angiotensin I isn’t very active on its own. It travels to your lungs, where it meets another enzyme called ACE (Angiotensin Converting Enzyme) . ACE changes Angiotensin I into Angiotensin II.
What are the roles of angiotensin II
Now, Angiotensin II is the boss! It does several important things:
It causes vasoconstriction, meaning it makes your blood vessels narrower. This increases your blood pressure.
It tells your adrenal glands to release Aldosterone
It tells your brain to make you feel thirsty and increases your “sympathetic drive” (making your body a bit more alert).
It also tells your pituitary gland to release Vasopressin (ADH), another hormone that helps you hold onto water.
Finally, Aldosterone acts on your kidneys to make them hold onto more salt (Na+ ) and water. This increases the amount of fluid in your blood, which also helps to raise blood pressure.
explain what happens with vasopressin and ADH
Stretch receptors in the left atrium
send continuous signals causes to
NTS. The NTS sends out inhibitory
nerves to the CVLM. CVLM signals
stimulate pituitary to release
vasopressin so stretching of the heart
inhibits this.
What triggers the release of vasopressin
What triggers the release of Vasopressin?
Dehydration or low blood volume: When you don’t have enough water or your blood volume drops, special sensors in your body detect this.
Increased osmolarity: This means your blood has a higher concentration of salts and other stuff, usually because you’re dehydrated.
Angiotensin II: Remember the RAAS system we just talked about? Angiotensin II also tells the brain to release vasopressin.
How is vasopressin released
How is Vasopressin released?
These signals (dehydration, low blood volume, high osmolarity, Angiotensin II) are sensed by your body and sent to a part of your brain called the hypothalamus.
The hypothalamus then tells another part of your brain, the posterior pituitary gland, to release the stored Vasopressin (ADH) into your bloodstream.
What are the two roles of vasopressin
1) Anti-diuresis (water saving): This is its primary role. When vasopressin reaches your kidneys, it tells them to put more “water channels” (called aquaporins) into their collecting tubes. This allows more water to move out of your urine and back into your blood. So, you pee less, and your body keeps more water.
2) Vasoconstriction: Vasopressin can also cause your blood vessels to narrow (constrict). This helps to increase your blood pressure.
Explain atrial natruiretic peptide (ANP)
ANP released by specialised atrial myocytes.
Secreted by increased filling pressures which stimulate stretch receptors.
Act at ANP receptors on vascular smooth muscle cells increasing cGMP
pathway (like nitric oxide).
Systemic vasodilatation – opposes action of noradrenaline, RAAS, ADH.
