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CVS > Control Of Blood Pressure > Flashcards

Control Of Blood Pressure Flashcards

1
Q

What is the equation for blood pressure?

A

Pressure = flow x resistance

  • mean arterial BP = CO x TPR
  • CO = SV x HR
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2
Q

Briefly explain the short way in which the body regulates blood pressure

A

Short term regulation:

– baroreceptor reflex (stretch when pressure changes- stretch more with high pressure and less with lower pressure)

– adjust sympathetic and parasympathetic inputs to the heart to alter cardiac output

– adjust sympathetic input to peripheral resistance vessels to alter TPR

  • Bradycardia and vasodilation counteract increased mean arterial pressure
  • The baroreceptor reflex works well to control acute changes in BP
  • Produces rapid response to CHANGES in BP
  • Does not control sustained increases because the threshold for baroreceptor firing resets
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3
Q

How is long term blood pressure controlled?

A
  • Complex interaction of neurohumoral responses
  • Directed at controlling sodium balance instead of heart rate etc and thus extracellular fluid volume
  • This is important for those who are hypertensive
  • helps when losing blood volume

• Plasma is part of the extracellular fluid compartment
– control of extracellular fluid volume controls plasma volume
– water follows Na+ therefore controlling total body Na+ levels controls plasma volume
- This has an effect on CO and SV

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4
Q

List the four parallel neurohumeral pathways that control circulating volume and hence BP

A
  1. Renin-angiotensin-aldosterone system
  2. Sympathetic nervous system
  3. Antidiuretic hormone (ADH)
  4. Atrial natriuretic peptide (ANP)
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5
Q

How do the four parallel neurohumoral pathways control circulating volume and hence BP?

A

Control BP in part by controlling sodium balance and extracellular fluid volume

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6
Q

Where is renin released from?

A

The juxtaglomerular apparatus (JGA) of the kidneys

JGA = macula densa + granule cells + surrounding mesangial cells

More specifically, Renin is released
from the granular cells of the afferent
arteriole in response to reduced perfusion pressure

These granular cells are next to the macula densa which detects low NaCl concentration

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7
Q

List 3 factors that stimulate renin release.

A

a) Reduced NaCl delivery to distal tubule in kidney

b) Reduced perfusion pressure in the kidney causes the release of renin
- also detected by baroreceptors in afferent arteriole

c) Sympathetic stimulation to JGA increases release of renin

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8
Q

What stimulates the JGA to release renin?

A
  • Decreased NaCl delivery to the macula densa
  • Sympathetic stimulation to juxtaglomerular apparatus
  • Decreased renal perfusion pressure (sensed by renal baroreceptors)
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9
Q

What is renin?

A

An enzyme that catalysts the break down of angiotensiogen to angiotensin 1

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10
Q

Outline the renin-angiotensin-aldosterone system

A

Angiotensinogen is broken down to angiotensin 1 by renin from the JGA granule cells.

Angiotensin 1 is converted to angiotensin 2 by ACE (angiotensin converting enzyme)

Angiotensin 2 has a direct effect on adrenal gland and stimulates release of aldosterone from adrenal cortex

Aldosterone stimulates Na+ reabsorption at the kidney

Vasoconstriction of the blood vessels

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11
Q

Angiotensin 2 has many significant clinical effects. What are they?

A

They act on Angiotensin 2 receptors AT1 and AT2

Main actions via AT1 receptor which is a G coupled receptor

It has a direct effect on adrenal gland and stimulates release of aldosterone from adrenal cortex

Aldosterone stimulates Na+ reabsorption at the kidney

Vasoconstriction of the blood vessels (arterioles)

Increased release of NA via the sympathetic outflow pathway

Increases thirst sensation (stimulates ADH release) from the hypothalamus

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12
Q

What is the action of aldosterone on the kidney?

A

AngII stimulates aldosterone release from the adrenal cortex Actions of aldosterone:

  • acts on principal cells of collecting ducts
  • stimulates Na+ and therefore water reabsorption

• activates apical Na+ channel (ENaC, Epithelial Na Channel) and apical K+ channel - so you lose K+
–>this is used as clinical clue

• also increases basolateral Na+ extrusion via Na/K/ATPase

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13
Q

What effect does ACE have on bradykinin?

A

ACE is particularly active within epithelial cells of lungs but is active in other parts of body too

It has effect in lung on breakdown of bradykinin

Bradykinin is broken down by ACE into peptide fragments

Bradykinin is a vasodilator so when broken down my ACE, vasodilation is reduced

The vasoconstriction effects of AngII are further augmented because ACE is also one of the kinase enzymes which breaks down the vasodilator bradykinin

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14
Q

How is the Brazilian Viper relevant to the Renin system?

A

When you get bitten by the viper, you get shocked, the bite releases anticoagulants and so your blood gets thinner and you lose some blood

It activate hypotension substances

Can cause coaguopathies which are little blood clots within blood vessels that consume all blood clotting products.

Can also lead to pulmonary oedema

Bradykinin potentiating factors in venom - it blocks the conversion of Ang1 to Ang2 - blocks ACE enzymes and so drops blood pressure

Needs to injected intravenously because if taken orally, gut will digest it

Clinically relevant:
This lead to drug development - ACE inhibitor = RAMAPRIL & CAPTOPRIL for long term hypertension usage

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15
Q

What are the effects of ACE inhibitors?

A

Block conversion of Ang1 to Ang2

Prevent the breakdown of bradykinin to peptide fragments

This leads to vasodilation and decrease in blood pressure

Side effect = dry cough cause by increase concentration of bradykinin

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16
Q

How does the sympathetic nervous system affect long term hypertension?

A

• High levels of sympathetic stimulation reduce renal blood flow
– Vasoconstriction of arterioles
– Less perfusion of renal arteries, less blood in glomeruli
- This activates NA+ retention so that water can follow
- Stimulates renin release from JGA cells

• Activates apical Na/H-exchanger and basolateral Na/K ATPase in PCT

• Stimulates renin release from JGcells
– leading to increased Ang II levels
– leading to increased aldosterone levels

• increased Na+ reabsorption

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17
Q

How do antidiretic hormones affect long term blood pressure?

A

• Main role is formation of concentrated urine by retaining water to control
plasma osmolarity
– Increases water reabsorption in distal nephron (AQP2)

• ADH release is stimulated by increases in
– plasma osmolarity
– or severe hypovolaemia (A decrease in the volume of blood in your body due to loss of blood or body fluid)

• Also stimulates Na+ reabsorption
– Acts on thick ascending limb
– stimulates apical Na/K/Cl co-transporter

• Also called arginine vasopressin
– Causes vasoconstriction

18
Q

How do natriuretic peptides affect blood pressure?

A
  • Atrial natriuretic peptide (ANP) promotes Na+ excretion
  • synthesised and stored in atrial myocytes
  • released from atrial cells in response to stretch - high pressure causes release of ANP
  • low pressure volume sensors in the atria

• reduced effective circulating volume inhibits the release of ANP to support
BP
– reduced filling of the heart – less stretch – less ANP released

19
Q

Describe the actions of ANP

A
  • Causes vasodilation of the afferent arteriole
  • Increased blood flow increases GFR
  • Also inhibits Na+ reabsorption along the nephron

• Acts in opposite direction to the other neurohumoral regulators
– Causes natriuresis (loss of sodium into urine)

• If circulating volume is low ANP release is inhibited
– This supports BP

20
Q

How do prostaglandins affect blood pressure?

A
  • Act as vasodilators
  • More important clinically than physiologically
  • Locally acting prostaglandins (mainly PGE2) enhance glomerular filtration and reduce Na+ reabsorption
  • May have important protective function
  • Act as a buffer to excessive vasoconstriction produced by SNS and RAA system sos that the blood vessel doesn’t start damaging itself
  • Important when levels of Ang II are high
21
Q

How does dopamine affect blood pressure?

A

• Dopamine is formed locally in the kidney from circulating L-DOPA

• Dopamine receptors are present on renal blood vessels and cells of Proximal Convoluted Tubule &
Thick Ascending Loop

• DA causes vasodilation and increases renal blood flow But not used as anti hypertensive

• DA reduces reabsorption of NaCl
– Inhibits NH exchanger and Na/K ATPase in principal cells of PCT and TAL

  • used clinically in Parkinson’s disease - reduces blood pressure
22
Q

What is hypertension?

A

Sustained increase in blood pressure

Stage 1 hypertension - ≥ 140/90 mmHg

Stage 2 hypertension - ≥160/100 mmHg

Severe hypertension - ≥ 180 systolic or ≥ 110 diastolic

Home BP should be lower than the clinical BP

If greater than or equal to 135/85 mmHg at home that is stage 1 hypertension

23
Q

What causes hypertension?

A

• In around 95% of cases the cause is unknown
– ‘essential’ or primary hypertension

• Where the cause can be defined it is referred to as secondary hypertension
– examples:
1) renovascular disease 
2) chronic renal disease
3) hyperaldosteronism 
4) Cushing’s syndrome

• With secondary hypertension – important to treat the primary cause

24
Q

What is accelerated hypertension?

A

Significant rise in blood pressure cause damages to blood vessels

No absolute value, just a significant rise

It’s a change in blood pressure

25
Q

What is essential or primary hypertension?

A

This means lots of different factors causing it

• No definable cause
– may be genetic factors 
– high BP tends to run in families
– environmental factors
– pathogenesis unclear
– recent research suggests dysfunction of DA receptors

• Sustained elevation of BP on three different separate occasions
– diastolic pressure > 90mmHg
– or systolic pressure > 140mmHg

26
Q

What is secondary hypertension?

A
  • Only accounts for a small percentage of cases
  • Identifiable pathological cause
  • Can treat the primary cause
27
Q

How does renovascular disease lead to secondary hypertension?

A

• Occlusion of the renal artery (renal artery stenosis) leads to renovascular disease

  • This causes a fall in
    perfusion pressure in that kidney

• Decreased perfusion pressure leads to increased renin production because since the kidney is not receiving enough blood, it thinks that the body is hypotensive

  • Thus the body works to counteract that
  • Activation of the renin-angiotensin-aldosterone system
  • Vasoconstriction and Na+ retention at other kidney
28
Q

How does renal parenchymal disease lead to secondary hypertension?

A

It is an umbrella term used for chronic kidney disease that leads to many secondary kidney issues

It can lead to scarring of the kidney

It is the most common cause of secondary hypertension

• Earlier stage may be caused by a loss of vasodilator substances

• In later stage Na+ and water retention due to inadequate glomerular filtration
- increase their plasma volume
– volume-dependent hypertension
- end up with smaller kidneys as it gets more and more scarred

29
Q

Outline how problems with the adrenal gland can lead to secondary hypertension?

A

• Conn’s syndrome – aldosterone secreting adenoma
– hypertension and hypokalaemia which is a clue for hypertension

• Cushing’s syndrome
– excess secretion of glucocorticoid cortisol - could be caused by a tumour of taking steroids at gym
– at high concentration acts on aldosterone receptors
- Na+ and water retention

• Tumour of the adrenal medulla
– phaeochromocytoma (colour rich tumours)
– secretes catacholamines (noradrenaline and adrenaline)

Not just in adrenal glad

30
Q

Why is it important to treat hypertension?

A

It is asymmptomatic

Although hypertension may be asymptomatic, it can have unseen damaging effects on:

– heart and vasculature

– potentially leading to heart failure, MI, stroke, renal failure and retinopathy

31
Q

Does diastolic or systolic BP affect BP differentially?

A

Yes, but only slightly

Link in systolic BP with hypertension is higher than that with diastolic BP

Rise in diastolic BP increases mortality
Rise in systolic BP increases mortality

And rise in both together increases it more significantly

32
Q

How does hypertension lead to so many vascular diseases?

A

It increases the work that the heart has to do

heart is pumping at higher pressure - after load

This leads to left ventricular hypertrophy–> heart failure

Increased after load also leads to increase in myocardial O2 demand –> myocardial ischaemia and MI

Hypertension also causes arterial damage which leads to atherosclerosis and weakened vessels.

Both can lead to cerebrospinal-vascular disease stroke, aneurysm, nephro-sclerosis and renal failure and retinopathy.

Meanwhile atherosclerosis can also cause myocardial ischaemia and MI.

33
Q

Which organs should doctors examine when a patient presents with hypertension?

A 
Brian
Eyes
Heart
Kidneys
Arteries
34
Q

Are BP treatments effective?

A

Yes, leads to a Significant reduction of mortality

35
Q

How do we treat hypertension?

A
  • For secondary hypertension – treat primary cause
  • Most cases no identifiable primary cause

• You can work out possible targets for treating hypertension from the
following equations
• BP = CO x TPR
• BP = SV x HR x TPR

36
Q

Outline some non-pharmalogical approaches to treating hypertension

A
  • Exercise
  • Diet
  • Reduced Na+ intake
  • Reduced alcohol intake
  • Lifestyle changes above can have limited effect
  • Failure to implement lifestyle changes could limit the effectiveness of antihypertensive therapy

(Smoking does not have a strong link with HT but has strong link with Cardiovascular disease)

37
Q

How would you target the renin-angiotensin-aldosterone system to treat hypertension?

A

• ACE inhibitors
– prevent production of Ang II from Ang I

  • Ang II receptor antagonists (AII antagonists)
  • Ang II is a powerful vasoconstrictor, it has fibrotic effects of heart and vessels has direct actions on the kidney and promotes the release of aldosterone, thus leading to NaCl and H2O retention
  • blocking production or action of AngII has diuretic and vasodilator effects

Generally use one or the other. Only rarely use both together.

38
Q

Which vasodilators can be used to treat hypertension?

A

• L-type Ca channel blockers
– reduce Ca2+ entry to vascular smooth muscle cells
– relaxation of vascular smooth muscle

• In principle could also use α1 receptor blockers
– reduce sympathetic tone (relaxation of vascular smooth muscle)
– can cause postural hypotension

39
Q

What is postural hypotension?

A

Postural hypotension: A drop in blood pressure (hypotension) due to a change in body position (posture) when a person moves to a more vertical position: from sitting to standing or from lying down to sitting or standing.

Postural hypotension is more common in older people.

The change in position causes a temporary reduction in blood flow and therefore a shortage of oxygen to the brain.

This leads to lightheadedness and, sometimes, a “black out” episode, a loss of consciousness.

40
Q

How are diuretics used for hypertension treatment?

A

Get rid of salt, and then get rid of fluids as water always follows

• Thiazide diuretics
– reduce circulating volume by reducing NA+ reabsorption

• Inhibit Na/Cl co-transporter on apical membrane of cells in distal tubule

• Other diuretics eg aldosterone antagonists (spironolactone) will also lower BP
– not first line choice

41
Q

Why are beta blockers less commonly used to treat hypertension? How do they work?

A

Using this to treat hypertension alone does not have the same positive effects that book the renin-angiotensin system does even though it reduces the production of renin. It’s moreso used in angina, when you want the heart to be slower and steadier

It works by blocking the beta 1 receptors in the heart in order to reduce sympathetic output

  • This leads to reduction in heart rate and contractility

It would only be used if there were other heart issues such as a previous MI or angina

CVS (11 decks)

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