S5) Control of Blood Pressure Flashcards
What is the formula for measuring blood pressure?
Pressure = flow x resistance
i.e maBP = CO x TPR
What are the two different ways of regulating blood pressure?
- Short term regulation
- Long term regulation
What does the baroreceptor reflex involve?
- Adjust sympathetic and parasympathetic inputs to the heart to alter CO
- Adjust sympathetic input to peripheral resistance vessels to alter TPR
What are the advantages and disadvantages of the baroreceptor reflex in terms of the control of blood pressure?
- 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
What are the principles governing the medium and longer term control of blood pressure?
- 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+)
Identify the four parallel neurohumoral pathways control circulating volume and hence BP
- Renin-angiotensin-aldosterone system (RAAS)
- Sympathetic nervous system (SNS)
- Antidiuretic hormone (ADH)
- Atrial natriuretic peptide (ANP)
Outline the Renin-angiotensin-aldosterone system
Where is renin released from?
Renin is released from granular cells of juxtaglomerular apparatus (JGA) in the afferent arteriole of the glomerulus
What stimulates renin released?
Renin release is stimulated by decreased circulating blood volume which reduces the perfusion pressure of the afferent arteriole
Explain which three factors stimulate renin release
What are the three effects of angiotensin II in RAAS?
- Vasoconstriction
- Stimulates release of aldosterone
- Na+ reabsorption at the kidney
What are the two different types of Angiotensin II Receptors?
- AT1
- AT2
The main action of angiotensin II is via AT1 receptor.
What type of receptor is this?
G-protein coupled receptor
Describe the specific actions of angiotensin II at the following sites:
- Arterioles
- Kidney
- SNS
- Adrenal cortex
- Hypothalamus
AngII stimulates aldosterone release from the adrenal cortex.
Describe the action of aldosterone on the kidney
⇒ 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
Relate the actions of Angiotensin converting enzyme and bradykinin
- 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
Explain the three ways in which the SNS controls blood pressure
- 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
When is ADH released?
- Increased plasma osmolarity
- Severe hypovolaemia
What is the main role of ADH?
ADH aims to form concentrated urine by retaining water to control plasma osmolarity
Explain the three ways in which ADH controls blood pressure
- Increases H2O reabsorption in distal nephron (AQP2)
- Stimulates Na+ reabsorption (stimulates apical Na/K/Cl co-transporter in thick ascending limb)
- Vasoconstriction
Atrial natriuretic peptides are synthesised and stored in atrial myocytes.
What stimulates and inhibits their release?
- Stimulated release: distension in atrial cells (greater blood volume)
- Inhibited release: reduced filling of heart (lesser blood volume
ANP acts in opposite direction to the other neurohumoral regulators.
Describe the two ways in which it controls blood pressure
- Vasodilates the afferent arteriole (increased GFR)
- Inhibits Na+ reabsorption along the nephron (natriuresis)
Explain how prostaglandins (mainly PGE2) act as a buffer to excessive vasoconstriction produced by SNS and RAAS
- Act as vasodilators
- Enhance glomerular filtration and reduce Na+ reabsorption
How is Dopamine formed?
Dopamine is formed locally in the kidney from circulating L-DOPA
Where are dopamine receptors found?
Dopamine receptors are present on renal blood vessels and cells of PCT & TAL
What effect does dopamine have on blood pressure?
- Vasodilation of afferent arteriole
- Reduces Na+ reabsorption (Inhibits Na+/H exchanger and Na/K ATPase)
What is hypertension?
Hypertension is the sustained increase in blood pressure
What are the different types of hypertension?
- Primary hypertension (95%) – cause is unknown
- Secondary hypertension (5%) – due to underlying condition
Classify hypertension into three different stages
In Essential hypertension, there is no clear identifiable cause.
Identify two possible influences
- Genetic factors
- Environmental factors
Provide four examples of common conditions which cause hypertension (secondary hypertension)
- Renovascular disease
- Chronic renal disease
- Hyperaldosteronism
- Cushing’s syndrome
In 4 steps, explain how renovascular disease leads to secondary hypertension
⇒ Renal artery stenosis reduces renal perfusion pressure in one kidney
⇒ Stimulated renin release
⇒ Activation of RAAS
⇒ Vasoconstriction and Na+ retention at other kidney
Explain the two ways in which renal parenchyma disease can lead to secondary hypertension
- Earlier stage: loss of vasodilator substances
- Later stage: Na+ and water retention due to inadequate glomerular filtration (volume-dependent hypertension)
What are the three adrenal causes for secondary hypertension?
- Conn’s syndrome
- Cushing’s syndrome
- Tumour of the adrenal medulla
Explain how Conn’s syndrome leads to secondary hypertension
- Aldosterone-secreting adenoma
- Hypertension and hypokalaemia ensues
Explain how Cushing’s syndrome leads to secondary hypertension
- Excess secretion of glucocorticoid cortisol
- High [cortisol] acts on aldosterone receptors
- Na+ and H2O retention
Explain how a tumour of the adrenal medulla can lead to secondary hypertension
Phaeochromocytoma – secretes catecholamines (noradrenaline and adrenaline) which increase sympathetic stimulation of kidneys and blood vessels
Outline the wide array of hypertension complications in terms of:
- Arterial damage
- Increased afterload
How does one treat secondary hypertension?
Treat the underlying pathological cause
Outline the treatment of hypertension with non-pharmalogical approaches
- Exercise
- Diet
- Reduced Na+ intake
- Reduced alcohol intake
Outline the treatment of hypertension by targeting RAAS
- ACE inhibitors
- AII receptor antagonists
Outline the treatment of hypertension with vasodilators
- CCBs
- α1 receptor antagonists (can cause postural hypotension)
Outline the treatment of hypertension with diuretics
- Thiazide diuretics – reduce circulating volume
- Aldosterone antagonists (spironolactone)
Why aren’t beta blockers often used for the treatment of hypertension alone?
Less commonly used to treat hypertension as blocking β1 receptors in the heart will reduce effects of sympathetic output (HR & contractility)
What are the target organs of clinical cardiovascular disease?
- Brain
- Eyes
- Heart
- Kidneys
- Arteries
