Control of vascular reactivity and blood pressure

what is vasculature

network of blood vessels in the body 

What is extrinsic influence on vascular function and why is it important?

• control of blood flow thorugh changing diameter of blood vessel by external factors (out of blood vessel)

• e.g controlled by neuranes or hormones

• important to maintain a contstant blood pressure and distribution of blood flow to organs and tissues

What is intrinsic influences on vascular function and why is it important?

• control of blood flow by changing the diameter of blood vessels controllde by local ingluences

• important to regulate distribution of blood flow to organs and tissue

how does the CVS idecrease heart rate 

how does CVS increase heart rate

how does CVS increase contrcatile force of the heart

how does the SNS do extrinsic controle of vasculature

• systematic arterioles are innervated by the SNS

• less firing of sympathetic neurons promotes

  vasodilatation instead of vasoconstriction

How is vasoconstriction caused by noradrenaline reinforced 

which out of noradrenline and adrenaline is more important for a1 activation and why

Noradrenaline has a higher affinity for α1 receptors than adrenaline,

therefore more important for α1 activation

what happens when adrenaline binds to B1, a1 and B2 recpetors 

when adrenline binds to b2 it promote selective vasodilatation of

specific tissues  during the fight or flight response

what happens when adrenline binds to b1 and a1 receptors 

How does the PNS extrinsically control vasculature?

• arterioles are innervated by the PNS but fewer than CNS 

• PNS causes vasodilatation in select vascular beds e.g fluid secretion, salivary glands, pancreas, intestinal mucosa, sex organs

what is TPR

Total Peripheral Resistance.

• It is the resistance of blood flow t through the blood vessels

•  TPR is a key factor in determining blood pressure as it affects how hard the heart has to work to pump blood throughout the body.

How do the effects of the PNS & SNS on the TPR vary?

• whilst PNS can redistribute blood flow within an organ/tissue, it isn't sufficient to affect TPR

• the SNS can redistribute blood flow within a tissue/between organs and if sufficient, SNS is stimulated & it will affect TPR

What does angiotensin IIpromote?

vasoconstriction

What does vasopressin(ADH) promote?

vasoconstriction & increased blood volume

What does atrial natriuretic peptide (ANP) do?

vasodilation

what are other extrinsit control of vascular functions apart from pns 

hormones

• Angiotensin II

• Vasopressin (antidiuretic hormone, ADH)

• Atrial natriuretic peptide (ANP)

Give examples of local factors that will affect local vascular tone?

Metabolites, local hormones, nitric oxide & prostacyclin

How do most arterioles respond to an increase in internal pressure and what type of response is this?

• Contraction - this reduces blood flow & capillary perfusion pressure (autoregulation)
  

• myogenic response

Why is this autoregulation important?

It protects important organs from increases in pressure

equation for flow

Flow = Pressure/Resistance

explain this graph showing autoregulatio

in a normal tube ( dashed line) as pressure increases  the flow increases 


in an autoregulated tube that hs a myogenic response as pressure increases it leads to constriction of the vessel reducign blood flow

role of histamine and how does it affect vascular tone?

•  released in response to inflammation or allergies

• causes an increase in vascular permeability

•  also causes release of nitric oxidewhich induces vasodilation

role of nitric oxide (NO) in regulation of blood pressure

• regulated by histamine

• stimulated by increase blood flow

• They activate the endothelial nitric oxide synthase in the endothelial lining of blood vessels which produces NO

• NO diffuses into smooth muscle cells and promotes vasodilation or prevents the constriction of the muscle cells

what is metabolic hyperaemia

when blood flow to a tissue increases because of a rise in its metabolic activity.

What is metabolic hyperaemia important in adn why

• cardiac & skeletal muscle: as they have increased metabolism

• Increased metabolism enhances production of substances which

  cause local vasodilatation of arterioles:

  H+, CO2, lactic acid, adenosine

• more blood flow to active muscle so its proportional to metabolic rate

What is reactive hyperaemia and whats its advantage ?

• If local blood flow is cut off, metabolites accumulate and cause vasodilatation

• wehn blood flow returns because fo vasodialtion the metabolietes and wate can quickly be removed

how does excersize make extrinsic and intrisinic influences to work togther

• intrinsic: the muscles make more Co2H+ and adenosine which all cause vasodialation 

• extrinsice: the SNS increases HR which leads to vasoconstriction to non essential areas so more blood to muscles 

what determines BP

• stroke volume and heart rate

• -TPR

•  central venous pressure and blood volume

what is acute regulation and what deos it happen via

•  the body's quick response to changes in blood pressure to keep it stable 

• Happens via the baroreceptor reflex

what are barorecptors 

• barorecptors are sensitve to stretch

• ↓ in blood pressure causes decrease in firing of baroreceptors

Describe the baroreceptor reflex when there is a decrease in blood pressure.

• decrease in the sending of signal to brain stems 

• increases the sympathetic drive 

• decrease in parasympathetic drive

• leads to widespread vasoconstriction, increased TPR, venoconstriction, increased CVP, HR, contractile force, cardiac output

• this restored BP

is BP the same for everyone

• resting BP changes with age and excersise 

What happens when we rapidly go from lying down to standing up?

• The main initial change on standing is gravity induced, causes pooling of blood in the lower limbs (about 500 ml in 15 s)

• This decreases central venous pressure (preload), and hence stroke volume

what is MABP 

mean arterial blood pressure 

Why is blood volume a major determinant of MABP?

Because it influences venous pressure, venous return, end diastolic volume (EDV), end diastolic pressure (EDP), SV & CO which all affect arterial pressure

How will an increase in blood volume affect MABP?

When blood volume increases, it causes mean arterial blood pressure (MABP) to rise. However, if this high pressure continues, the kidneys respond by removing extra salt and water, which reduces blood volume and brings MABP back down to normal.

what controls blood volume 

• Blood volume is controlled by osmolality (plasma needs to be osmotically balanced)

• I.e. if our plasma is very salty so hyperosmotic - cells will lose their water and shrink and become damage.

• If we place our cells in watery solution (hypoosmotic) - cells will swell and burst and become damaged.

What happens when you have an increase in plasma osmolality?

• Osmoreceptors in hypothalamus detect ↑ plasma osmolality

• Triggers thirst so more water intake

• ADH ( AKA vasopressin) released from posterior pituitary → binds to V2 receptors

• Causes aquaporins to insert in distal nephron leading to increase in water reabsorption

• Plasma osmolality returns to normal

What is osmolality

measure of the concentration of dissolved particles (like salts and sugars) in a solution

are osmoreceptors sensitive?

• very sensitive because it is critical we maintain plasma osmolarity with a narrow range to stop damage

What senses blood volume?

• Stretch receptors

• Pressure natriuresis

How can pressure natriuresis sense and regulate blood volume?

1. when blood volume is too high, it increases arterial pressure, 

2. leads to increase in local metabolite release in the renal artery,

3.  leads to increase in blood flow in the renal medulla  

4. this leads to increase excretion of Na 

5. water also excrete

how do stretch receptors sense and regulate blood volume

• increase in blood volume affects the central venous pressure which is detected ny stretch receptors in the artia and venoatria junction

• this makes 2 responses, hormonal and nervous 

• hormonal: this makes atrial natriuretic peptide ( ANP) release from atrial myocytes

• this increases urine production and sodium ion excretion 

• nervous: decrease in sympathetic activity decreases MABP and decrease renal sympathetic stimulation which decreases renin-angiotensin system (RAAS) activation

what is syncope

It is fainting.

• There is vasovagal or neurocardiogenic syncope

  • Vasovagal syncope is the more commonly used term and refers to fainting caused by a trigger, like emotional stress, pain, or standing for too long.

  • Neurocardiogenic syncope is a broader term that includes vasovagal syncope and emphasizes the role of the nervous and cardiovascular systems in causing the fainting.

• Syncope can be triggered by the sight of blood or needles

• Vasovagal syncope essentially overrides the fight or flight response

How does vasovagal syncope override the fight or flight response and cause fainting?

how are the glomerulus and juxtaglomerular apparatus important in regulating blood volume

• regulates via RAAS

• a decrease in blood volume will increase  renal sympathetic drive promoting afferent constriction and renin release from juxtaglomerular cells in afferent arteriole

• Renin converts angiotensinogen to angiotensin 1

• Which is then converted into Angiotensin 2 by angiotensin converting enzyme (ACE) 

• angiotensin 2 is a Potent vasoconstrictor

  Stimulates ADH release promoting water reabsorption

  Stimulates adrenals to release aldosterone (Na+ reabsorption)

State the steps of what happens when there is an increase in blood volume

1. Increase in blood volume

2. Detected by atria stretch receptors

3. Which is sensed by hypothalamus in brain stem

4. Leads to a decrease in ADH release and decrease in sympathetic renal nerve activity

5. Together this promotes an increase in diuresis which decreases renin and ang2 and a decrease in aldosterone

6. ANP is also released by atrial stress

7. This all leads to a decrease in Na+ and water reabsorption

8. Volume restored