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Urinary > Renal Control Of Blood Pressure And CO > Flashcards

Renal Control Of Blood Pressure And CO Flashcards

0
Q

Where are baroreceptors found?

A

Aortic arch

Carotid sinuses

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1
Q

What is used for short term control of BP? How does it work?

A

Baroreceptor reflex
Nerve endings are sensitive to stretch caused by increased arterial pressure
Send signal along afferent pathway to medulla
Signals down efferent pathway adjust sympathetic input which adjusts TPR
Adjusts sympathetic and parasympathetic inputs to heart to alter cardiac output

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2
Q

How is the sympathetic NS used in long term renal control of BP?

A

High levels of sympathetic stimulation reduce renal blood flow by vasoconstriction (α1 receptor)
Decrease in GFR -> decrease in Na+ excretion
Activates apical Na-H exchanger and NaKATPase in PCT
Stimulates renin release

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3
Q

What are the ways for long-term control of BP?

A

Sympathetic nervous system
Natriuretic peptides
RAAS
ADH

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4
Q

What does atrial natriuretic peptide (ANP) do?

A

Promotes Na+ excretion
Causes vasodilatation of afferent arteriole, increasing GFR
Inhibits Na reabsorption along the nephron

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5
Q

Where is ANP synthesised and stored?

A

Atrial myocytes

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6
Q

What causes release and inhibition of release of ANP?

A

Stimulates release - Stretch
Inhibits release - low pressure volume sensors in atria detect reduced effective circulating volume (reduced filling of the heart)

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7
Q

Where is renin released from?

A

Granular cells of juxtaglomerular apparatus

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8
Q

What causes release of renin?

A

Reduced perfusion pressure in the kidney which is detected by baroreceptors in the afferent arteriole
Decreased NaCl concentration at the macula densa (due to low GFR) causes sympathetic stimulation to the JGA, increasing renin release.

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9
Q

Action of renin?

A

Increases BP

Converts angiotensin to angiotensin I

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10
Q

What receptors does angiotensin II act on?

A

AT1 (mostly) (GPCR)

AT2

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11
Q

Actions of angiotensin II?

A

Arterioles - vasoconstriction by working on smooth muscle cells, increasing TPR and BP. Also constricts afferent arteriole in kidney

Kidneys - enhanced Na+ reabsorption in PCT by stimulating NaH exchanger

Sympathetic NS - increases release of NA

Adrenal cortex - release of aldosterone

Hypothalamus - increased thirst sensation by stimulating ADH release

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12
Q

Action of aldosterone?

A

Acts on intracellular receptors

Increases expression of apical Na+ channel (ENaC) and NaKATPase in principal cells of collecting duct

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13
Q

What works against aldosterone?

A

Spironolactone

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14
Q

What stimulates release of ADH

A

Increases in plasma osmolarity

Severe hypovolaemia

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15
Q

What is the main role of anti-diuretic hormone?

A

Formation of concentrated urine by retaining water
Stimulates Na reabsorption
Acts on thick ascending limb to stimulate Na-K-Cl co-transporter (therefore less water can leave thin ascending limb due to less of a gradient)

16
Q

How is ADH released?

A

Baroreceptors detect a 5-10% drop in BP
Signals to brain stem via vagus nerve
Modulates sympathetic nerve outflow
Secretion of ADH (and reduction of ANP)

17
Q

Overall action of ANP?

A

Decrease BP

18
Q

What do prostaglandins do?

A

Vasodilation
Locally - enhance glomerular filtration and reduce Na reabsorption
Act as a buffer to excessive vasoconstriction by sympathetic NS and RAAS
Important when angiotensin II is high

19
Q

Overall action of prostaglandins?

A

Reduce blood pressure

20
Q

What is pathway involved in the formation of prostaglandins? What can interfere with it?

A

Cyclo-oxygenase (COX) pathway

NSAIDS

21
Q

When can administration of NSAIDs be dangerous? Why?

A

When renal perfusion is compromised
They can further decrease GFR
Cause acute renal failure
Due to inhibition of prostaglandins

In heart failure/hypertensive patients, can worsen condition by increasing NaCl and water retention

22
Q

What is hypertension?

A

Sustained increase in blood pressure

23
Q

What is essential hypertension and what proportion of cases does this make up?

A

Where there is no definable cause

95% of cases

24
Q

What factors could play a part in essential hypertension?

A

Genetic

Environmental

25
Q

What are some causes of secondary hypertension?

A

Renovascukar and chronic renal disease
Aldosteronism
Cushing’s syndrome

26
Q

How can renovascular disease lead to hypertension?

A

Renal artery stenosis
Fall in perfusion pressure in that kidney
Detected as a low circulating volume
Increased renin production
Activation of RAAS
Vasoconstriction and Na+ retention in other kidney

27
Q

How can renal parenchymal disease lead to hypertension?

A

Can cause a loss of vasodilator substances eg prostaglandins and dopamine (earlier stage)
Later stage - Na and water retention due to inadequate glomerular filtration
Leads to volume dependent hypertension

28
Q

What is Conn’s syndrome and how does it lead to hypertension?

A

Have an aldosterone-secreting adenoma

Causes hypertension and also hyperkalaemia

29
Q

How does Cushing’s syndrome lead to hypertension?

A

Excess secretion of cortisol

At high concs, acts on aldosterone receptors causing Na and water retention

30
Q

How can pheochromocytoma lead to hypertension?

A

It is a tumour of the adrenal medulla

Secretes catecholamines such as NA and adrenaline

31
Q

What can hypertension lead to?

A 
Heart failure
Stroke
MI
Renal failure
Retinopathy
32
Q

For treating hypertension, how is the RAAS targeted?

A

Use of ACE-inhibitors or angiotensin II receptor antagonist

Blocking ang II has diuretic and vasodilator effects

33
Q

How can diuretics be used to reduce blood pressure and which ones?

A

Thiazide - reduces circulating volume by inhibiting Na-Cl transporter in distal tubule
Spironolactone

34
Q

Mechanism of action of drug vasodilators?

A

Block L-type calcium channels
Reduce Ca entry into smooth muscle cells
Relaxation of smooth muscle

Also have alpha-1 receptor blockers which reduce sympathetic tone

35
Q

How do β blockers work?

A

Block β1 receptors in the heart to reduce effects of sympathetic output
Reduces heart rate and contractility

36
Q

What are some non-pharmacological approaches for reducing hypertension?

A

Exercise
Diet
Reduce Na intake
Reduce alcohol

37
Q

What does dopamine do?

A

Dopamine receptors found on renal blood vessels and PCT
Increases renal blood flow
Reduces reabsorption of NaCl

Urinary (19 decks)

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