Control of Blood Pressure Flashcards
What is the equation of pressure, and thus what is the equation of mean arterial blood pressure
Pressure = flow x resistance
Mean arterial blood pressure = CO x TPR
Explain the baroreceptor reflex
As arterial pressure increases, it feeds back to medulla oblongata and has a negative sympathetic effect
Adjusts sympathetic input to peripheral resistance vessels to alter TPR
Nerve endings in the carotid sinus and aortic arch are sensitive to stretch
Increased arterial pressure stretches these receptors
Decreased pressure stretches less
Explain the renin-angiotensin-aldoesterone system
- Renin is released from granular cells of juxtaglomerular apparatus (JGA)
- Renin converts angiotensinogen to angiotensin I
- ACE (angiotensin converting enzyme) converts angiotensin I to angiotensin II
- Angiotensin II causes vasoconstriction, stimulates sodium reabsorption at kidney and stimulates aldosterone release from adrenal cortex
Two types of angiotensin II receptors - AT1 and AT2
Main actions via AT1 receptor - G-protein coupled receptor - Aldosterone acts on principal cells of collecting ducts
Release absorbs sodium and causes potassium release from apical channels
Increases basolateral sodium extrusion through Na/K-ATPase
Clinical sign is low blood potassium
Explain the factors that stimulates renin release
Reduced NaCl delivery to distal tubule
Reduced perfusion pressure in the kidney causes the release of renin (reduced circulating volume)
Detected by baroreceptors in afferent arteriole
Sympathetic stimulation to JGA increases release of renin
Explain the use of ACE inhibitors
Used to reduce blood pressure
Block production of angiotensin II and lead to build up of bradykinin
Bradykinin causes dry cough (vasodilator actions)
How does the sympathetic nervous system affect blood pressure through kidneys
High levels of sympathetic stimulation reduce renal blood flow
Vasoconstriction of arterioles
Decrease glomerular filtration rate - lower Na excretion
Activates sodium retention - activate Na/H exchanger on apical side and Na/K-ATPase on basolateral side
Stimulates renin release from JG cells
How does ADH affect blood pressure control
Formation of concentrated urine by retaining water to control plasma osmolarity
ADH release stimulated by increases in plasma osmolarity (dehydration) or severe hypovolaemia
Also stimulates sodium reabsorption on ascending limb
Also known as arginine vasopressin - causes vasoconstriction
How do natriuretic peptides affect blood pressure control
ANP promotes sodium secretion
Synthesised and stored in atrial myocytes
Released from atrial cells in response to stretch - low pressure volume sensors in atria
Reduced effective circulating volume inhibits the release of ANP to support blood pressure
Reduced filling of the heart leads to reduced stretching and reduced ANP release
ANP causes vasodilation of the afferent arteriole
Increased blood flow increases glomerular filtration rate
Inhibits sodium reabsorption within nephron
Acts opposite direction to other neurohormonal regulators - cause natriuresis (loss of sodium in urine)
Explain the effect of prostaglandins on blood pressure
Vasodilator, enhance glomerular filtration and reduce sodium reabsorption, protective function of local blood vessels at times of stretch
Explain the effect of dopamine on blood pressure
Vasodilator, used in Parkinson’s disease
Define the stages of hypertension
Primary hypertension - no definable cause
Genetic, environmental factors,
Sustained blood pressure about 140/90 mmHg
Accelerated hypertension - significant rise in blood pressure causes severe damage to blood vessels
Secondary hypertension - when the cause can be defined
Renovascular disease, chronic renal disease, hyperaldosteronism, Cushing’s syndrome
Over 160/100mmHg
Severe hypertension - over 180/110 mmHg
Explain some causes of secondary hypertension on organs in the body
Renovascular disease - occlusion of the renal artery causes a fall in perfusion pressure in that kidney
Leads to increased renin production and activation of renin-angiotensin-aldosterone system
Vasoconstriction and sodium retention at other kidney
Renal parenchymal disease - earlier stage may be loss of vasodilator substances
Later stage, sodium and water retention due to inadequate glomerular filtration
Adrenal causes
Conn’s syndrome - aldosterone secreting adenoma (hypertension and hypokalaemia)
Cushing’s syndrome - excess secretion of glucocorticoid cortisol
High concentration acts on aldosterone receptors - sodium and water retention
Tumour of the adrenal medulla (phaeochromocytoma) - secretes catecholamines
Explain the effect of hypertension on tissue and organs within the body
Hypertension increases heart afterload and arterial damage
Increase in heart afterload leads to left ventricular hypertrophy and then heart failure
Also increases myocardial oxygen demand leading to ischaemia and MI
Arterial damage leads to atherosclerosis and weakened vessels
Both lead to cerebrovascular disease, stroke, aneurysm, nephrosclerosis & renal failure retinopathy
What are common treatments of hypertension
For secondary hypertension - treat primary cause
Non-pharmacological approaches - exercise, diet, reduced sodium intake, reduced alcohol intake, lifestyle changes
ACE inhibitors, Ang II receptor antagonists (vasodilator effects)
L-type Ca channel blockers - reduce Ca entry to vascular smooth muscles cells and relax it (vasodilation)
α1 receptor blockers - reduce sympathetic tone
Diuretics - reduce sodium reabsorption and circulating volume
