Session. 5.2 Flashcards
What is hypertension?
A sustained increase in blood pressure
What’s the difference between primary and secondary hypertension?
Primary/ essential = unknown cause
Secondary = known cause
What are the effects of increased afterload with hypertension?
- left ventricular hytrophy = heart failure
- increased myocardial oxygen demand = myocardial ischaemia and MI
What are the effects of arterial damage with hypertension?
- atherosclerosis = MI and myocardial ischaemia
Atherosclerosis and weakened vessels will also lead to
- cerebrovascular disease stroke
- aneurysm
- nephroscleorisis and renal failure
- retin-opathy
What are the main organs damaged by hypertension?
Brain Eyes Kidneys Arteries Heart
What regulates blood pressure in the short term?
Tachycardia to try maintain lower BP vice versa with bradycardia
Barorceptor reflex = doesn’t control sustained increases as threshold for baroreceptor firing resets.
What factors stimulate renin release in the renin angiotensin aldosterone system (RAAS)?
1) reduced NaCl delivery to distal tubule
2) reduced perfusion pressure in the kidney causes the release of renin
3) detected baroreceptor in afferent arterial (decreased pressure)
4) sympathetic stimulation juxtaglomerular apparatus increases release of renin
Juxtaglomerular apparatus release renin
What is the role of renin in the renin angiotensin aldosterone system (RAAS)?
Angiotensin — renin—> angiotensin 1
Angiotensin 1 — ACE —> angiotensin 2
ACE = angiotensin converting enzyme
What is the angiotensin 2 receptor and what will the effect be of ang 2?
Main actions via AT1 receptor but also AT2 GCPR
Causes
- vasoconstriction
- Na+ reabsorption at kidney as stimulates aldosterone release
- increases release of NA
- increases thirst sensation (stimulates ADH release)
What is the action of aldosterone on the kidney???
- acts on principal cells of collecting ducts
- stimulates Na+ and therefore water reabsorption
- activates apical Na+ channels, and apical K+ channel
- also increase basolateral Na+ extrusion via Na/K/ATPase
What else does ACE do outside of the RAAS system?
ACE is also a kiniase enzyme which breaks down the vasodilator bradykinin into peptide fragments
What will stop the effect of ACE?
ACE inhibitors
Have a diuretic and vasodilator effect
NB: can also use angiotensin receptor blockers for ang II receptors
How can the sympathetic nervous system affect blood pressure?
High levels of sympathetic stimulation reduce renal blood flow
- vasoconstriction of arterioles
- decrease GFR
Stimulates renin release from cells of afferent arteriole
Stimulates Na+ reabsorption in proximal tubule
How can ADH affect blood pressure?
- increase water reabsorption in distal nephron = produce concentrated urine
- stimulated by increase in plasma osmolarity
- stimulates Na+ reabsorption (and water leaves with Na+)
What are the actions of atrial natriuretic peptide?
- Cause vasodilation of afferent arteriole
- Increased blood flow increases glomerular filtration rate
- Also inhibits Na+ reabsorption along the nephron
- Acts in opposite direction to other neurohumoral regulators
- If blood pressure is low ANP release is inhibited
