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*CVS Jeny > S5) Control of Blood Pressure > Flashcards

S5) Control of Blood Pressure Flashcards

1
Q

What is the formula for measuring blood pressure?

A

Pressure = flow x resistance

i.e maBP = CO x TPR

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2
Q

What are the two different ways of regulating blood pressure?

A
  • Short term regulation
  • Long term regulation
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3
Q

What does the baroreceptor reflex involve?

A
  • Adjust sympathetic and parasympathetic inputs to the heart to alter CO
  • Adjust sympathetic input to peripheral resistance vessels to alter TPR
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4
Q

What are the advantages and disadvantages of the baroreceptor reflex in terms of the control of blood pressure?

A
  • Advantages: controls acute changes in BP and produces rapid responses to changes
  • Disadvantage: doesn’t control sustained increases because the threshold for baroreceptor firing resets
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5
Q

What are the principles governing the medium and longer term control of blood pressure?

A
  • Complex interaction of neurohumoral responses directed at controlling Na+ balance and thus extracellular fluid volume
  • Control of extracellular fluid volume controls plasma volume (H2O follows Na+)
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6
Q

Identify the four parallel neurohumoral pathways control circulating volume and hence BP

A
  • Renin-angiotensin-aldosterone system (RAAS)
  • Sympathetic nervous system (SNS)
  • Antidiuretic hormone (ADH)
  • Atrial natriuretic peptide (ANP)
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7
Q

Outline the Renin-angiotensin-aldosterone system

A
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8
Q

Where is renin released from?

A

Renin is released from granular cells of juxtaglomerular apparatus (JGA) in the afferent arteriole of the glomerulus

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9
Q

What stimulates renin released?

A

Renin release is stimulated by decreased circulating blood volume which reduces the perfusion pressure of the afferent arteriole

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10
Q

Explain which three factors stimulate renin release

A
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11
Q

What are the three effects of angiotensin II in RAAS?

A
  • Vasoconstriction
  • Stimulates release of aldosterone
  • Na+ reabsorption at the kidney
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12
Q

What are the two different types of Angiotensin II Receptors?

A
  • AT1
  • AT2
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13
Q

The main action of angiotensin II is via AT1 receptor.

What type of receptor is this?

A

G-protein coupled receptor

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14
Q

Describe the specific actions of angiotensin II at the following sites:

  • Arterioles
  • Kidney
  • SNS
  • Adrenal cortex
  • Hypothalamus
A
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15
Q

AngII stimulates aldosterone release from the adrenal cortex.

Describe the action of aldosterone on the kidney

A

⇒ Acts on principal cells of collecting ducts

⇒ Stimulates Na+ reabsorption (thus, H2O)

⇒ Activates apical Na+ channel (ENaC) and apical K+ channel

⇒ Increases basolateral Na+ extrusion via Na/K/ATPase

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16
Q

Relate the actions of Angiotensin converting enzyme and bradykinin

A
  • Bradykinin has vasodilator actions
  • ACE (aka kininase II) converts angiotensin I to angiotensin II & breaks down bradykin into further augment the vasoconstriction effect of AngII
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17
Q

Explain the three ways in which the SNS controls blood pressure

A
  • Increased sympathetic stimulation reduces renal blood flow (afferent vasoconstriction, increase GFR and Na+ excretion)
  • Stimulates Na+ reabsorption in PCT (apical Na/H-exchanger and basolateral Na/K ATPase)
  • Sympathetic stimulation of renin release from JGA
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18
Q

When is ADH released?

A
  • Increased plasma osmolarity
  • Severe hypovolaemia
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19
Q

What is the main role of ADH?

A

ADH aims to form concentrated urine by retaining water to control plasma osmolarity

20
Q

Explain the three ways in which ADH controls blood pressure

A
  • Increases H2O reabsorption in distal nephron (AQP2)
  • Stimulates Na+ reabsorption (stimulates apical Na/K/Cl co-transporter in thick ascending limb)
  • Vasoconstriction
21
Q

Atrial natriuretic peptides are synthesised and stored in atrial myocytes.

What stimulates and inhibits their release?

A
  • Stimulated release: distension in atrial cells (greater blood volume)
  • Inhibited release: reduced filling of heart (lesser blood volume
22
Q

ANP acts in opposite direction to the other neurohumoral regulators.

Describe the two ways in which it controls blood pressure

A
  • Vasodilates the afferent arteriole (increased GFR)
  • Inhibits Na+ reabsorption along the nephron (natriuresis)
23
Q

Explain how prostaglandins (mainly PGE2) act as a buffer to excessive vasoconstriction produced by SNS and RAAS

A
  • Act as vasodilators
  • Enhance glomerular filtration and reduce Na+ reabsorption
24
Q

How is Dopamine formed?

A

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

25
Q

Where are dopamine receptors found?

A

Dopamine receptors are present on renal blood vessels and cells of PCT & TAL

26
Q

What effect does dopamine have on blood pressure?

A
  • Vasodilation of afferent arteriole
  • Reduces Na+ reabsorption (Inhibits Na+/H exchanger and Na/K ATPase)
27
Q

What is hypertension?

A

Hypertension is the sustained increase in blood pressure

28
Q

What are the different types of hypertension?

A
  • Primary hypertension (95%) – cause is unknown
  • Secondary hypertension (5%) – due to underlying condition
29
Q

Classify hypertension into three different stages

A
30
Q

In Essential hypertension, there is no clear identifiable cause.

Identify two possible influences

A
  • Genetic factors
  • Environmental factors
31
Q

Provide four examples of common conditions which cause hypertension (secondary hypertension)

A
  • Renovascular disease
  • Chronic renal disease
  • Hyperaldosteronism
  • Cushing’s syndrome
32
Q

In 4 steps, explain how renovascular disease leads to secondary hypertension

A

⇒ Renal artery stenosis reduces renal perfusion pressure in one kidney

⇒ Stimulated renin release

⇒ Activation of RAAS

⇒ Vasoconstriction and Na+ retention at other kidney

33
Q

Explain the two ways in which renal parenchyma disease can lead to secondary hypertension

A
  • Earlier stage: loss of vasodilator substances
  • Later stage: Na+ and water retention due to inadequate glomerular filtration (volume-dependent hypertension)
34
Q

What are the three adrenal causes for secondary hypertension?

A
  • Conn’s syndrome
  • Cushing’s syndrome
  • Tumour of the adrenal medulla
35
Q

Explain how Conn’s syndrome leads to secondary hypertension

A
  • Aldosterone-secreting adenoma
  • Hypertension and hypokalaemia ensues
36
Q

Explain how Cushing’s syndrome leads to secondary hypertension

A
  • Excess secretion of glucocorticoid cortisol
  • High [cortisol] acts on aldosterone receptors
  • Na+ and H2O retention
37
Q

Explain how a tumour of the adrenal medulla can lead to secondary hypertension

A

Phaeochromocytoma – secretes catecholamines (noradrenaline and adrenaline) which increase sympathetic stimulation of kidneys and blood vessels

38
Q

Outline the wide array of hypertension complications in terms of:

  • Arterial damage
  • Increased afterload
A
39
Q

How does one treat secondary hypertension?

A

Treat the underlying pathological cause

40
Q

Outline the treatment of hypertension with non-pharmalogical approaches

A
  • Exercise
  • Diet
  • Reduced Na+ intake
  • Reduced alcohol intake
41
Q

Outline the treatment of hypertension by targeting RAAS

A
  • ACE inhibitors
  • AII receptor antagonists
42
Q

Outline the treatment of hypertension with vasodilators

A
  • CCBs
  • α1 receptor antagonists (can cause postural hypotension)
43
Q

Outline the treatment of hypertension with diuretics

A
  • Thiazide diuretics – reduce circulating volume
  • Aldosterone antagonists (spironolactone)
44
Q

Why aren’t beta blockers often used for the treatment of hypertension alone?

A

Less commonly used to treat hypertension as blocking β1 receptors in the heart will reduce effects of sympathetic output (HR & contractility)

45
Q

What are the target organs of clinical cardiovascular disease?

A
  • Brain
  • Eyes
  • Heart
  • Kidneys
  • Arteries

*CVS Jeny (17 decks)

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