Control of blood pressure Flashcards
Short term regulation
Baroreceptor reflex
Baroreceptor reflex adjusts:
- Sympathetic and parasympathetic inputs to the heart to alter cardiac output
- Sympathetic input to peripheral resistance vessels to alter TPR
Where are baroreceptors found?
Carotid sinus and aortic arch
Where do the baroreceptors signal to?
Medulla
Longer term control of blood pressure
- Complex interaction of neurohumoral responses
- Directed at controlling sodium balance and thus extracellular fluid volume
- Therefore control of plasma volume
Four parallel neurohumoral pathways controlling circulating volume
- Renin angiotensin aldosterone system
- Sympathetic nervous system
- Antidiuretic hormone (ADH)
- Atrial natriuretic peptide (ANP)
Renin is released from
- Released from granular cells of juxtaglomerular apparatus (JGA)
Factors that stimulate renin release
- Reduced NaCl delivery to kidney
- Reduced perfusion pressure in kidney (detected by baroreceptors in afferent arterial)
- Sympathetic stimulation to JGA increases release of renin
Effects of angiotensin II
- Stimulates aldosterone (from adrenal cortex)
- Stimulates Na+ reabsorption at kidney
- Vasoconstriction
Angiotensin II receptors
- AT1(main action) and AT2
- G protein coupled receptor
Angiotensin II receptor sites and action: Arterioles, sympathetic NS, hypothalamus
- Vasoconstriction
- Increased release of noradrenaline
- Increases thirst sensation (stimulates ADH release)
Action of aldosterone on the kidney
- Acts on principle cells of collecting ducts
- Stimulates Na+ reabsorption
- Activates apical Na+ channel (ENaC, Epithelial Na Channel) and apical K+ channel
- (therefore high aldosterone = low K+)
- Increases basolateral Na+ extrusion via sodium potassium pump
What does angiotensin converting enzyme (ACE) also break down?
Bradykinin, a vasodilator
Effects of using ACE inhibitors
A dry cough, due to accumulation of bradykinins
Examples of ACE inhibitors
Ramipril, Lisinopril, Perindopril, Enalapril
Sympathetic stimulation effect on renal blood flow
- Vasoconstriction of arterioles
- Decreased glomerular filtration rate so decreased Na+ excretion
Role of sympathetic nervous system in maintaining blood pressure
- High levels of sympathetic stimulation reduce renal blood flow
- Activates apical Na/H exchanger and basolateral Na/K ATPase in proximal convoluted tube
- Stimulates renin release from JGcells
Antidiuretic hormone effects on blood pressure
- Increases water reabsorption in distal nephron (AQP2) to control plasma osmolarity
- ADH release is stimulated by increases in plasma osmolarity or sever hypovolaemia
- Stimulates Na+ reabsorption via apical Na/K/Cl cotransporter
- Also called arginine vasopressin, causes vasoconstriction
Natriuretic peptide control on blood pressure
- Atrial natriuretic peptide (ANP) promotes Na+ excretion
- Synthesised and stored in atrial myocytes
- Released from atrial cells in response to stretch
- Reduced effective circulating volume inhibits release of ANP to support BP (reduced filling of heart, less stretch, less ANP released)
Actions of ANP
- Causes vasodilation of the afferent arteriole
- Increased blood flow increases glomerular filtration rate
- Inhibits Na+ reabsorption along the nephron
- Causes natriuresis (loss of sodium into urine)
- If circulating volume is low ANP release is inhibited
