Control Of Blood Pressure And Hypertension Flashcards
What is the normal adult blood pressure?
Between 90/60mmHg and 120/80mmHg
What is hypertension?
Sustained increase in blood pressure > 140/90mmHg
What causes hypertension?
In 95% of cases, the cause is unknown - primary hypertension
Referred to as secondary hypertension if cause can be defined e.g. renovascular disease, chronic renal disease, hyperaldosteronism, Cushing’s syndrome
Give some examples of diseases attributable to hypertension
Heart failure, stroke, cerebral haemorrhage, chronic kidney failure, hypertensive encephalopathy, retinopathy, peripheral vascular disease, aortic aneurysm, LV hypertrophy, MI, CHD
How is blood pressure regulated?
Pressure = flow x resistance
Mean arterial BP = CO x TPR
CO = stroke volume x HR
Both short and long term regulation.
Short term regulation - baroreceptor reflex - adjust sympathetic and parasympathetic inputs to the heart to alter CO, adjust sympathetic input to peripheral resistance vessels to alter TPR
Where are the main baroreceptors found?
Carotid sinus
Aortic arch
Describe the baroreceptor reflex
Baroreceptors detect increased mean arterial pressure -> afferent pathway to medulla oblongata -> efferent pathway to heart and vessels -> bradycardia and vasodilation counteract increased mean arterial pressure
Describe the baroreceptor reflex
Baroreceptors detect increased mean arterial pressure -> afferent pathway to medulla oblongata -> efferent pathway to heart and vessels -> bradycardia and vasodilation counteract increased mean arterial pressure
(RAAS) what are the factors that stimulate renin release?
Reduced NaCl delivery to distal tubule. Reduced perfusion pressure in the kidney causes the release of renin - detected by baroreceptors in afferent arteriole. Sympathetic stimulation to juxtaglomerular apparatus increases release of renin
What are the 4 parallel neurohumoral pathways controlling circulating volume and hence BP?
RAAS
Sympathetic nervous system
ADH
ANP
(RAAS) What enzyme converts angiotensinogen to angiotensin I?
Renin (from juxtaglomerular granule cells)
(RAAS) What enzyme converts angiotensin I to angiotensin II?
ACE (angiotensin converting enzyme)
Angiotensin II:
leads to vasoconstriction
Stimulates Na+ re absorption at kidney
Stimulates aldosterone (from adrenal cortex) (which also stimulates Na+ re absorption at kidney)
(RAAS) What are the actions of aldosterone on the kidneys?
Acts on principal cells of collecting ducts
Stimulates Na+ and therefore water re absorption
Activates apical Na+ channel and apical K+ channel
Increases basolateral Na+ extrusion via Na/K ATPase
(RAAS) What is another action of ACE (aka kininase II)?
Other than converting angiotensin I to angiotensin II, ACE also breaks down bradykinin into peptide fragments.
Vasoconstriction effects of AngII are further augmented because ACE is also one of the kininase enzymes which breaks down the vasodilator bradykinin
(RAAS) How do ACE inhibitors lower blood pressure?
Inhibit actions of ACE
Therefore no actions of angiotensin II -> less reabsorption of Na+ and therefore water
And bradykinin isn’t broken down -> vasodilation
How does the sympathetic nervous system control circulating volume and blood pressure
High levels of sympathetic stimulation reduces renal blood flow - vasoconstriction of arterioles, decrease GFR -> decrease Na+ excretion
Activates apical Na/H-exchanger and basolateral Na/K ATPase in proximal convoluted tubule.
Stimulates renin release from juxtaglomerular cells - leading to increased AngII levels -> increased aldosterone production - increased Na+ reabsorption
How does ADH affect blood pressure?
- Formation of concentrated urine by retaining water to control plasma osmolarity
- ADH release is stimulated by increases in plasma osmolarity or severe hypovolaemia
- Stimulates Na+ reabsorption
- Aka arginine vasopressin - causes vasoconstriction
How do natriuretic peptides control BP?
- atrial natriuretic peptide (ANP) promotes Na+ excretion
- synthesised and stored in atrial myocytes
- released from atrial cells in response to stretch
- 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
What are the actions of ANP?
Causes vasodilation of the afferent arteriole
Increased blood flow increases GFR
Inhibits Na+ reabsorption along the nephron
Acts in opposite direction to the other neurohumoral regulators - causes natriuresis
If circulating volume is low, ANP release is inhibited -> supports BP
What are prostaglandins?
Act as vasodilators
Important clinically
Locally acting prostaglandins enhance glomerular filtration and reduce Na+ reabsorption
Acts as a buffer to excessive vasoconstriction produced by SNS and RAAS
Important when levels of Ang II are high
What are the effects of dopamine?
Causes vasodilation and increases renal blood flow
Reduces reabsorption of NaCl - by inhibiting NH exchanger and Na/K ATPase in principal cells of PCT and TAL
What is renovascular disease?
Causes secondary hypertension
Occlusion of the renal artery - causes a fall in perfusion pressure in that kidney
Decreased perfusion pressure leads to increased renin production
Activation of RAAS
Vasoconstriction and Na+ retention at other kidney
What is renal parenchymal disease?
Causes secondary hypertension
Earlier stage may be a loss of vasodilator substances
In later stage, Na+ and water retention due to inadequate glomerular filtration - volume-dependent hypertension
What are the adrenal causes of secondary hypertension?
Conn’s syndrome - aldosterone secreting adenoma -> hypertension and hypokalaemia
Cushing’s syndrome - excess secretion of glucocorticoid cortisol - at high concentration acts on aldosterone receptors - Na+ and water retention
Tumour of the adrenal medulla - phaeochromocytoma - secretes catecholamines
