Session 4 - BP and the Kidney Flashcards
How is mean arterial blood pressure calculated?
1/3 systolic + 2/3 diastolic BP
Where are baroreceptors found in the body?
Aortic arch
Carotid sinus
How is RAAS activated at the kidney?
Renin released at juxta-glomerular apparatus by granular cells in response to:
- Reduced NaCl delivery to distal tubule (macula densa)
- Reduced perfusion pressure in kidney (detected by baroreceptors at afferent arteriole)
- Sympathetic stimulation to JGA >renin release.
How does the RAAS system increase blood pressure?
Find RAAS diagram and try to draw out!
What actions does angiotensin II have at the kidney?
- Vasoconstriction of efferent and afferent arterioles (more effect on efferent)
- Enhanced Na+ reabsorption at PCT (stimulates Na-H exchanger in apical)
- Stimulate aldosterone release (adrenal cortex) : (affects principle cells of CD)
- Stimulate ADH release from post. pituitary (Stimulate aquaporins in CD)
What are the actions of aldosterone on the kidney?
- Acts on Principal cells of collecting duct.
- Stimulating Na+, thus water reabsorption.
- Activates apical ENaC (and apical K+ channel)
- Increases basolateral Na+ extrusion via Na/K ATPase.
In which ways does the sympathetic nervous system stimulate the kidneys?
- High levels of SNS stimulation reduce renal blood flow.
- Vasoconstriction of arterioles,
What causes prostaglandin release at the nephron, what affect does this have?
Release stimulated by: - Angiotensin II - Noradrenaline - Anti-diuretic hormone Locally released, causing vasodilation of afferent arteriole (very local effect). Also enhance renin release.
How does antidiuretic hormone cause increase in blood pressure?
Increases water reabsorption in the distal nephron, via aquaporin channels (AQP2).
What stimulates the release of ADH?
Increase in Plasma osmolality (detected a hypothalamus).
Severe hypovolaemia.
What are the main actions of Atrial natriuretic peptide?
- Vasodilation (systemic & afferent arteriole of glomerulus - >GFR)
- Inhibits Na+ reabsorption especially in collecting duct. > Loss of sodium.
How does ANP reduce blood pressure?
Its action opposes that of the RAAS system.
feedback to Adrenal glands, and inhibits renin secretion
What is hypertension?
Persistent increase in blood pressure.
How is hypertension clinically diagnosed?
Three readings of blood pressure above 140/90.
or 135/85 for 24 hour home monitoring device
Which diseases can cause secondary hypertension?
Renovascular hypertension.
Coarctation of the aorta.
Primary hyperaldosteronism (Conn’s Syndrome)
Cushing’s syndrome.
What are the two main types of Renovascular disease?
75% are Atheroma. Fibromuscular dysplasia (FMD) = a non-atherosclerotic, non-inflammatory disease of the blood vessels that causes abnormal growth within the wall of an artery. (commonly renal/ carotid)
What are the differences caused in unilateral vs bilateral renal artery stenosis?
Unilateral
- Increased RAAS from kidney on stenotic side.
- Causes hypertension, but healthy kidney can compensate and increase Na (and H20) excretion.
(no fluid overload!)
Bilateral
- Both stenotic vessels, so both kidneys have reduced GFR.
- This decrease in GFR will mean impaired Na and water secretion, thus increased Arterial BP.
- This increase BP will mean RAAS is actually inhibited (maybe due to ANP?), as there is no normal kidney to remove excess. This means angiotensin levels will be low or normal.
(There is hypertension, and can be oedema)
What is coarctation of the aorta?
A congenital narrowing of the aorta (usually where the ductus arteriosus joined the aorta)
How can an aortic coarctation be diagnosed?
Radioradial pulse delay, or radiofemoral delay.
Dependent on which two arteries there is a delay in can give an idea of the location of the coarctation
What are some main endocrine causes of hypertension?
- Primary hyperaldosteronism (Conn’s syndrome) e.g. adrenal hyperplasia/ adenoma.
- Cushing’s syndrome
What would circulating levels of Renin and Angiotensin II be in Primary hyperaldosteronism.
Low
aldosterone would cause high Na+ and water reabsorption, increasing BP, inhibting RAAS