Blood Pressure and The Kidney Flashcards
Which two organs are intimately related to regulate blood pressure?
heart and kidney
Outline how RAAS works.
Low BP stimulates JGA to release renin. Renin converts angiotensinogen–> angiotensin1 ACE will then convert angiotensin 1–> angiotensin 2 Angiotensin 2 causes vasoconstriction Angiotensin 2 stimulates adrenal glands to release aldosetrone. Aldosterone promotes Na+ and water reabsorption in the kidney
What four thing will help the kidney deal with poor perfusion?
RAAS SNS Prostaglandins ADH
If the perfusion in the kidney rises what peptide will be released in response?
ANP
recall the equation for mean arterial pressure?
SV x HR x TPR
How can the kidney effect cardiac out put?
Increase in circulating blood volume will increase the SV
Recall from CVS the short term control of blood pressure.
Baraoreceptor reflex - adjust heart rate (SAN) and force (myocytes) of contraction by the ANS via the medulla oblongata. Symathetics will effect vascular tone to adjust TPR Thirst is also stimulated
How does the kidney control BP changes more long term?
Thirst Increase NaCl and water reabsorption So over all it acts to increase circulating volume
How does the kidney control BP changes more long term?
Thirst Increase NaCl and water reabsorption So over all it acts to increase circulating volume (increase ECF)
Where are the baroreceptors?
Aortic Arch and carotid sinus
What 3 factors stimulate RAAS?
Reduced NaCl delivery to distal tubule Reduced perfusion pressure in kidney Sympathetic stimulation of the JGA
Which cells release renin?
Juxtaglomerular granular cells of the afferent arteriole in response to poor perfusion
What 3 components make up the juxtaglomerular apparatus?
Macula Densa, granule cells and surrounding mesangial cells
Where are the macula densa?
Glomerular edge of DCT - detects changes in [NaCl] stimulates renin release
List the effects of angiotensin 2.
Activates sympathetics– vasoconstriction ADH release Thirst Stimulates adrenal cortex to release aldosterone
How does angiotensin 2 effect the kidney.
vasoconstriction of efferent>afferent (preserve GFR in low perfusion) PCT absorbs more na+ as NA-H stimulated collecting duct stimulated by ADH and aldosterone (indirect effect)
Which RAAS receptor is in the PCT?
AT2
What are the effects of aldosterone?
Acts on principle cells of CD- stimulates Na (and H2O) reabsorption by increasing expression of apical ENaC and K+ channels Also upregulates basolateral Na/K ATPase to get the sodium into the blood for water to follow
What would high levels of sympathetic innervation do to GFR?
Lots of vasoconstriction would decrease GFR because renal blood flow would drop
What effect does sympathetic innervation have in the kidney?
Apical Na/H exchanger activated Na/K ATPase activated Renin released from JGA
Why do we need prostaglandins when we have lost of sympathetic stimulation, ADH and RAAS activation?
Protect the kidney for excessive vasoconstriction leading to hypoxia in the kidney
Normally whats the effect of prostaglandins in the kidney?
Minimal
What is the local action of prostaglandins in the nephron?
Afferent arteriole dilation (lets blood flow to avoid hypoxia - increases filtration pressure gradient to conserve GFR)
What is the effect of local prostaglandin release on renin?
Local prostaglandin release STIMULATES renin release
What does ADH do in times of low blood volume?
Forms concentrated urine by increasing H2O reabsorption in the distal nephron (more AQP2 channels) Also tightens vessels (vasopressin is the other name)
What stimulates ADH release?
Hypovolaemia or increase in osmolality of plasma (it needs diluting)
If blood pressure acutely increases- how does the body respond?
Baroreceptor reflex Renal autoregulation- to avoid huge increase in GFR ANP
What are the two types of renal auto-regulation?
Myogenic Tubulo-glomerular feedback
With in what range of mean arterial BP can renal autogregulation control GFR?
80-180
What is tubule-glomerular feedback and how does it aid increasing BP?
GFR up Macula densa detects higher [NaCl] Paracrine to afferent arteriole - constriction stimulated GFR down
What are the 2 major actions of ANP?
Vasodilation and Inhibition of Na+ reabsorption in the CD
How does ANP increase GFR?
If circulating volume is high ANP secreted. Vasodilation systemically and of the afferent arteriole increases GFR. Na+ reabsorption goes down so you get a nature’s Diuresis
What mechanisms do we as humans favour- the ones that increase BP or reduce?
Increase (historically thats what we needed)
Why do we get persistent hypertension?
abnormality between arterial pressure and renal salt and water excretion (pressure-naturesis)
name the two pathological processes that involve RAAS and BP
Secondary hypertension Oedema (secondary hyperaldosteronisms)
Name the four types of secondary hypertension
Renovascular hypertension Coarctation of the aorta Primary hyperaldosteronism Cushings
What would you need to consider when working out if hypertension is primary or secondary.
>95% are primary Young patient, especially females with a borderline low potassium- investigate secondary causes
What is renovascular disease?
Poor renal perfusion because of renal artery pathology- stenosis or narrowing. Caused by atheroma (75%), fibromuscular dysplasia or rarer ones. Can be unilateral or bilateral
Why might a kidney with renovascular disease be small?
Ischaemia from lack of blood flow leads to shrunken kidney
Outline how renovascular disease leads to secondary HTN
Perfusion to kidney reduced Kidney tries to compensate by increasing blood volume- RENIN released. Angiotensin 2 levels rise Vasconstriction and aldosterone released Hypertension
Why in primary aldosteronism is Renin low but aldosterone high?
The adrenal is affected so anything down stream of the adrenal is upregulated but anything higher is lower than expected.
List the endocrine causes of hypertension that involve RAAS
Primary Aldosteronsim
Cushing’s Syndrome
Liquorice (minerolaocorticoid excess)
Which endocrine causes of HTN are independent of RAAS?
Phaeochromocytoma
Acromegaly
Thyroid problems
What happens if one kidney suffers renovascular disease?
The affected kidney will increase RAAS
The unaffected kidney will get hyper-perfused and act to counter act this- induce naturesis and supress RAAS
List 3 clinical signs of coarctation of the aorta?
Hypertension
Radio-femoral delay
Low BP in legs
(note- normal U&E normal)
What leads to a primary hyperalosteronism?
Adrenal adenoma
Adrenal hyperplasia
How do you diagnose someone with primary hyperaldosteronism?
Measure the aldosterone:renin
Look for adenoma on CT
How might you treat a primary hyeraldosteronism?
Surgery to remove adenoma
If surgery isn’t an option then block aldosterone (mineralocorticoid antagonists)
How does liquorice effect the distal nephron?
Inhibits the enzyme that degrades cortisol to cortisone.
If high cortosl persists it will bine mineralocortiocoid recptors and give similar effects to aldosterone
Why are Cushings patients hypertensive?
Cortisol binds mineralocorticoid recepetor
Reabsorb more sodium (means we have lose K+ remember) and water will follow the sodium
Why do we get oedema?
Excess salt and water in interstitium
List causes of oedema
How at the cpaillary bed might you get oedema?
Increase in vascular hydrostatic pressure
Albumin leaks to interstitium (oncotic pull of interstitium goes up)
Blocked lymphatics- non pitting
Nephrotic syndorm- loss of protein in urine so reduced vacular oncotics
What is the difference betwenn transudate and exudate?
Trasudate- fluid leaks
Exudate - fluid and protein leak
What 3 factors effect the effective arterial blood pressure?
Cardiac output
Intravascular volume
Systemic Vascular Resistance
Why do we retain water in heart failure?
The heart pump is no longer effective.
Renal blood flow drops- Kidney acts to increase blood Volume (sympathetic, juxtaglomerular feedback and RAAS)- water and sodium retained
Effective circulatory volume dropped becaue pump failed so volume receptor in left atrium and throaci vessel drops- ADH secreted to retain water
How might a chronic kindey disease pateint develope oedema?
How do nephrotic syndrome pateints get oedema?
Nephrotic syndrome- leads to proteinuria so reduced vascular oncotic pressure– Kidney compensates to increase blood volume as its getting poorly perfused
Reduced GFR from kindey damage
What is the clinical triad for a nephrotic syndrome?
Proteinuria >350mg/mmol
Hypoalbunaemia
Oedema
Minimal change disease is a common cause of nephrotic syndrome in children, why do they get oedema?
Reduced effective arterial blood volume
GFR tends to be ok
