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APP > The control of systemic arterial blood pressure > Flashcards

The control of systemic arterial blood pressure Flashcards

1
Q

How is BP regulated in the short-term?

A

Baroreflex

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2
Q

Short-term - closed or open system?

A

Closed

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3
Q

What receptors are involved in the short-term response and what do they monitor?

A

high-pressure baroreceptors located in the aortic arch and carotid sinus, which monitor the systemic pressure and the pressure of blood being delivered to the brain respectively

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4
Q

Describe how baroreceptors work

A

Nerve endings expressing channels such as TRP - thought to be mechanosensitive stretch receptors where activation → influx of cations (Na+ and Ca2+) → depolarisation

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5
Q

High BP - baroreceptor firing high or low?

A

High

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6
Q

What are the carotid sinus baroreceptors innervated by?

A

sinus nerve of Herin, a branch of the glossopharyngeal nerve

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7
Q

What are the aortic arch baroreceptors innervated by?

A

Aortic nerve which then combines with the vagus nerve

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8
Q

Draw table comparing properties of the baroreceptors

A

OneNote

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9
Q

What do patients with baroreflex failure present with?

A
  • orthostatic hypertension
  • recurrent syncope (caused by drop in blood flowing to brain)
  • volatile hypertension
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10
Q

Where do baroreceptors project to?

A

Cardiovascular centre in medulla

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11
Q

Where do most afferents from baroreceptors project to?

A

NTS, which sends interneurons to various brainstem centres

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12
Q

Describe circuitry surround NTS and draw diagram from OneNote

A

Diagram
• Baroreceptor afferents secrete excitatory glutamate onto the GluR2 subunits of AMPA receptors on NTS interneurons, exciting them…
- INHIBITORYinterneurons project onto, and inhibit thevasomotor area of the ventrolateral medulla; includesA1andC1areasin the rostral VL area, as well as the inferior olive and other nuclei(C1 area neurons have tonic output which normally elicits vasoconstriction; this is inhibited by the NTS input)

  • EXCITATORYinterneurons project onto theCardioinhibitory areawhich includes thenucelus ambiguus anddorsal motor nucleus of the vagus(These neurons are excited to elicit bradycardia through parasympathetic action on the heart)
  • INHIBITORYinterneurons project onto thecardioacceleratory areain thedorsal medulla(When stimulated, these cause heart rate and contractility to increase)
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13
Q

What is the overall result of baroreceptor stimulation?

A

Depression in:

  • vessel tone
  • heart rate
  • contractility
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14
Q

Effectors of decreased BP on the heart/cardiac nerves

A

Na → SAN = increases HR and contractility
through beta1
- look at last year’s cardio deck for more

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15
Q

Effects of decreased BP on adrenal medulla

A

Preganglionic sympathetic neurons release ACh onto nAChRs on the adrenal medulla to stimulate Adr release into circulation, by exocytosis (of stored Adr) -chromaffin cells

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16
Q

Effects of decreased BP on blood vessels

A

VASOCONSTRICTION
- • Terminals release NA onto VSM which acts on two different types of adrenoreceptor
• Adrenaline is in circulation from the adrenal medulla
• The overall effect will depend on the Adr/NA ratio (Adr binds with higher affinity to B receptors, NA binds with higher affinity to A receptors)
• Will also depend on the receptor populations
• B2 receptors are Gs coupled - cause vasodilation
○ PKA mediated phosphorylation of MLCK (inactivation)
• A1 receptors are Gq coupled - cause vasoconstriction
IP3 mediated Ca release, form more Ca-calmodulin to activate MLCK

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17
Q

Is there any parasympathetic innervation of the vasculature?

A

No

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18
Q

How may body temp alter systemic BP?

A

§ Hypothermia - increased sympathetic flow to cutaneous blood vessels - vasoconstriction – reducing heat loss via radiation at the skin surface - BP rises
§ Conversely, relief of sympathetic innervation in hyperthermia - vasodilation in periphery to promote heat loss via radiation - overall systemic BP drops – can faint
§ Shows how local fluctuation in BP in extremities can affect whole BP

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19
Q

Discuss resetting of baroreceptors

A

It appears that exercise training (e.g. in athletes) resets the BR so its activation threshold is higher - allows greatly increase HR, BP, sympathetic activity during exercise

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20
Q

What is the most important factor in long-term control of BP?

A

the need for the kidneys to balance fluid volume intake with volume output

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21
Q

What is natriuresis?

A

process of sodium excretion in the urine through the action of the kidneys

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22
Q

Describe pressure-natriuresis relationship of the kidney

A

natriuresis and so the volume of fluid excreted increases with increasing perfusion pressure

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23
Q

If the pressure-natriuresis curve was unmodified by other factors, why would blood pressure increase with increased salt and water intake?

A

• This is because increased fluid intake increases effective circulating volume (ECV), which increases central venous pressure (CVP); this increases atrial filling and ventricular filling and thereby increases myocardial contractility and stroke volume according to Starling’s law
The resulting increase in CO leads to a rise in ABP, which increases renal perfusion pressure, allowing the extra volume to be eliminated and thereby maintaining volume homeostasis

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24
Q

What does the RAAS act to do?

A

Prevent appreciable changes in blood pressure even with large changes in salt and water intake

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25
Q

Describe RAAS

A

After increased volume intake, hence increased BP, renal perfusion pressure and thus GFR increases (as described):
• This reduces the time available for NaCl reabsorption by NKCC2 transporters in the TAL of LoH, thereby increasing NaCl delivery to the macula densa
• Macula densa cells detect this increased NaCl concentration
• Macula densa cells accumulate intracellular Na+ - causes the cell to swell due to water influx down its osmotic gradient - opening of basolateral stretch-activated anion channels - increases ATP leakage - ATP converted to adenosine, which binds to Gi-coupled A1 (adenosine) receptors and inhibits renin secretion from granular cells
• Moreover, afferent arteriole stretch and β1 receptor stimulation also both decrease renin release
• Conversely, in times of lowered BP, renin secretion increases
• Renin = a protease which cleaves the liver-derived angiotensinogen to form AI (angiotensin I) - which is further cleaved by ACE to generate AII (angiotensin II)

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26
Q

Does renin increase or decrease with lowered BP?

A

Increase

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27
Q

Does renin increase or decrease with highered BP?

A

Decrease

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28
Q

What does AII act on?

A

s shown, AII induces aldosterone secretion from the adrenal cortex
○ Aldosterone acts on the MR receptors of principal cells in the DCT and the proximal part of the CD, where it upregulates transcription of the basolateral Na+/K+-ATPase, as well as the apical ENaC 🡪 increases sodium and water reabsorption

-AII 2 also = arteriolar vasoconstriction and ADH secretion for H2O reabsorption

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29
Q

What is phaeochromocytoma?

A

Phaeochromocytoma is an adrenal medullary tumour in which there is excess adrenaline secretion. This causes overactivation of the RAAS, and consequent long-term hypertension.

30
Q

What is Conn’s syndrome?

A

○ Hyperaldosteronism, caused by adrenal cortical tumour

excess Na+ and water reabsorption - hypertension; oedema; and K+ loss - muscle weakness and hypokalaemia

31
Q

What is Addisons syndrome?

A

Adrenal cortical failure

Low aldosterone secretion - hypotension and hyperkalaemia

32
Q

Effect of ANP on blood pressure

A

• High ECV causes overloading of the atria - stretch of atrial myocytes, causing them to release ANP
• ANP primarily acts through cGMP-mediated effects to ultimately cause natriuresis + subsequently diuresis
• E.g. ANP inhibits renin release from the macula densa
+ causes dilation of the afferent arterioles and constriction of the efferent arterioles to increase GFR and thus uresis

33
Q

Read through Guyton model stuff now!

A

OneNote

34
Q

Draw Guyton model of closed circulation

A

OneNote

35
Q

What is the Bayliss effect?

A

The Bayliss effect in vascular smooth muscles cells is a response to stretch. This is especially relevant in arterioles of the body. When blood pressure is increased in the blood vessels and the blood vessels distend, they react with a constriction; this is the Bayliss effect. Stretch of the muscle membrane opens a stretch-activated ion channel. The cells then become depolarized and this results in a Ca2+ signal and triggers muscle contraction

36
Q

Who has a predisposition to HBP?

A

Black and Indian people than white and Chinese people

37
Q

Why is HBP likely to occur with increased age?

A
  • reduction of compliance of vasculature
  • could be due to an increase in collagen content, covalent cross-linking of collagen, elastin fracture, calcification, reduction in elastin content
  • luminal diameter is also reduce
38
Q

Define compliance

A

Change in volume for a given change in pressure

39
Q

Why are black people more likely to have a high blood pressure?

A

They have a lower nephron mass compared with the rest of the population
They are more likely to posses an ENaC mutation which makes the channel hyperactive which explains low renin hypertension in commonly found in black people

40
Q

What blood pressure do you have to have to be regarded as hypertensive?

A

> 140/90

41
Q

What is the normal BP range?

A

90-120

42
Q

Symptoms of hypertension

A

Rarely has any immediate ones - usually asymptomatic

43
Q

Describe the difference between primary and secondary hypertension

A
  • Primary → no clear cause

- Secondary → clear endocrine or renal cause and arises in younger individuals (there are a number of known causes)

44
Q

What may be the mechanism of hypertension in obese individuals? What does this do to the pressure natriuresis curve?

A

It has been found that the sympathetic nerve activity, especially in the
kidneys, is increased 2- to 3-fold in overweight individuals, which may
provide the mechanism of increased risk: sympathetic nerve activity
stimulates renin release, resulting in greater production of AII and
aldosterone, hence increased sodium reabsorption. This shifts the pressure-
natriuresis curve to the right, so that a greater arterial pressure is needed to
excrete the volume of fluid taken in.

45
Q

List the risk factors of primary hypertension

A
  • age
  • afro-caribbean
  • chronic high salt intake
  • obesity
  • smoking
  • alcohol
  • lack of exercise
46
Q

List the causes of secondary hypertension

A
  • Arterial hypertension of the vessels supplying the kidney (arterial stenosis) → reduced GFR → RAAS activation
  • Damage to the nephrons of the kidney/surgical resection in kidney mass
  • Fibromuscular dysplasia → reduced GFR → RAAS activation
  • Excess aldosterone (Conn’s) → excess Na+ reabsorption
47
Q

What are the three main organs at risk during hypertension?

A
  • heart (enhances risk of atherosclerosis through sheer stress, rupture of plaques leading to ischaemic heart disease and strokes, cardiac hypertrophy)
  • brain - stroke
  • kidneys - disruption of glomeruli - progressive renal failure
48
Q

Draw the NICE guidelines pathway for hypertension treatment

A

OneNote

49
Q

Give examples of ACE inhibitors

A

Captopril and ramipril

50
Q

What do ACE inhibitors do?

A

These inhibit ACE, hence preventing conversion of AI to AII, therefore preventing the
downstream effects of AII.

51
Q

Side effects of ACE?

A
  • persistent dry cough due to accumulation of bradykinin (ACE due to accumulation of bradykinin), dizziness, postural hypotension
52
Q

What are the three groups of Ca2+ channel blocker?

A

1 - phenulalkylamines (e.g. verapamil)
2 - dihydropyridines (e.g. nifedipine)
3 - benzothiazepines (e.g. diltiazem)

53
Q

Which group of Ca channel blockers are most commonly used as antihypertensives? Why?

A

Dihydropyridines → they have the greatest selectivity for vascular smooth muscle cells

54
Q

How do Ca channel blockers reduce hypertension?

A

blocking L type Ca2+ channels
reducing Ca2+ influx
VSMC relaxation

55
Q

What do thiazides do? Give an example.

A

Hydrochlorothiazide

Inhibit NCC1 in the DCT and so impair sodium reabsorption

56
Q

Side effects of thiazides

A 
Orthostatic hypotension
Hypokalemia 
Hyponatremia 
Hypercalcaemia 
hyperuricaemia (too much uric acid in blood)
Metabolic acidosis
57
Q

Discuss the mechanism by which diuretics is general may lower blood pressure

A

Diuretics have traditionally been thought of as lowering BP by reducing circulating volume;
however, according to the model of the role of the kidneys in long-term control of blood pressure
outlined in this essay, their primary effect may be reduction of sodium reabsorption, shifting the
pressure-natriuresis curve to the left, with reduction in ECV being secondary to this.

58
Q

Give an example of an alpha1 blocker

A

Prazosin

59
Q

What are the side effects of alpha blockers?

A

orthostatic hypotension, syncope, and very rarely priapism (prolonger erection)

60
Q

Discuss role beta blockers may play in reduction of hypertension

A

These were originally thought to act by reducing cardiac output through antagonising the
positive chronotropic and inotropic effects of sympathetic cardiac stimulation.
 However, their main mode of action is now thought to be antagonism of sympathetically-
stimulated renin release from granule cells; this reduces AII and aldosterone levels, shifting
the pressure-natriuresis curve to the left.
Drugs that block central sympathetic outflow such as the α2 agonists (e.g. clonidine) which
are mainly used in hypertension during pregnancy, may also act via this mechanism (as well
as by possible vasodilation of afferent arterioles).

61
Q

List the main classes of drug used to treat hypertension

A

Diuretics:

  • Thiazide
  • loop
  • potassium-sparing

Vasodilators:

  • Alpha-adrenoceptor antagonists (alpha-blockers).
  • ACE inhibitors
  • Angiotensin receptor blockers (ARBs).
  • Ganglionic blockers (in acute hypertensive emergencies).
  • Nitic oxide donors (in acute hypertensive emergencies).

Ion channel modulators:

  • Ca2+-channel blockers
  • K+-channel openers.
  • Renin inhibitors.

Cardio-inhibitory drugs:

  • Beta-blockers.
  • Ca2+-channel blockers.
  • Centrally acting sympatholytic drugs
62
Q

What can we do in the case of drug-resistance hypertension?

A

1- ablation of renal artery afferent and efferent nerves
2. chronic carotid baroreflex stimulation
3 - DBS - neurones in the centrolateral PAG matter

63
Q

What do loop diuretics act on?

A

NKCC2 in thick ascending limb

  • inhibit sodium, choline and potassium reabsorption
  • NKCC2 inhibition at the macula densa also reduces Na transported into maculadensa cells - stimulates the release of renin - increase fluid retention
64
Q

What do calcium-sparing diuretics refer to?

A

Drugs that cause diuresis without causing K+ loss in urine leading to hypokalemia

65
Q

What may be used instead of ACE inhibitors for A part of treatment?

A

Angiotensin receptor blockers (e.g. losartan) and renin antagonists

66
Q

Discuss ganglionic blockers

A
  • inhibit transmission between preganglionic and postganglionic neurones in the autonomic nervous system, often acting as nicotinic receptor antagonists
67
Q

How do NO donors work? What is the mechanism of NO?

A

Activate guanylate cyclase and increase intracellular levels of cGMP which leads to vasodilation

68
Q

Describe centrally-acting sympatholytics

A

Centrally acting sympatholytics block sympathetic activity by binding to and activating alpha2 (α2)-adrenoceptors. This reduces sympathetic outflow to the heart thereby decreasing cardiac output by decreasing heart rate and contractility. Reduced sympathetic output to the vasculature decreases sympathetic vascular tone, which causes vasodilation and reduced systemic vascular resistance, which decreases arterial pressure

69
Q

Example of alpha2 adrenoreceptor agonist?

A

Clonidine

70
Q

Describe K+ channel openers

A
  • Open ATP-sensitive K+ channels in vascular smooth muscle
  • causes hyperpolarisation of smooth muscle
  • this closes voltage-gated calcium channels and. decreases intracellular calcium
  • less calcium to bind to calmodulin
  • less activation of MLCK and phosphorylationof myosin light chain
  • relaxation and vasodilation

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