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Human Physiology and Pharmacology > Week 19: Monitoring and Control of Blood Pressure > Flashcards

Week 19: Monitoring and Control of Blood Pressure Flashcards

1
Q

What controls arterial blood pressure?

A

CO
Total peripheral resistance (TPR)
Blood volume

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2
Q

What regulates arterial blood pressure?

A 
Neuronal mechanisms (short-term)
Hormonal mechanisms (long-term)
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3
Q

What is a baroreceptor?

A

pressure sensitive receptors

Relay info to the brain (afferent)

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4
Q

Why are baroreceptors important?

A

sense blood pressure and relay the info to the brain so proper bp can be maintained

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5
Q

Where are baroreceptors located?

A

located in the carotid sinus and in the aortic arch

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6
Q

What happens when a baroreceptor detects a change in blood pressure?

A

projects nerve fibres to the brain stem cardiovascular centre.

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7
Q

What does the baroreceptor reflex consist of? (5) in order

A
  • A detector- BaroR
  • Afferent pathways
  • A co-ordinating centre
  • Efferent neural pathways –> relay output of coordinating centre to the periphery
  • Effectors –> execute and appropriate response and alter the controlled variable, correcting deviation form set point.
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8
Q

What is hypotension?

A

low blood pressure

–> background AP has fallen at baroreceptor

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9
Q

What is hypertension?

A

High blood pressure

background firing rate at baroreceptors increase

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10
Q

From where does the firing come from in a baroreceptor reflex and where doe sit report to?

A

Frequency of firing in the baroR from aortic arch and carotid sinus that report to the cardiovascular centre in the brain where the ongoing second to second bp is.

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11
Q

What section does the baroR discharge AP?

A

systole –> normotensive

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12
Q

What causes cyclic changes in neuronal activity?

A

cardiac contraction and relaxation

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13
Q

What is the effect of the co-ordinating centre in the BaroR Reflex?

A

– in the CNS. Compares signal detected in the periphery to a set-point and generates an error message

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14
Q

What can decrease increased bp?

A

bradycardia and vasodilation

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15
Q

What do the efferent neurones effect?

A

heart an vessels

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16
Q

Why do we feel light-headed when we stand up?

A

the alpha-adrenoR present in smooth muscle of lower limb drops when we lie down and drop transiently when we stand up

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17
Q

What is the effect of the afferent nerves when heart rate is increased from the baroreceptor?

A

increased AP frequency in response to increased bp

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18
Q

Where does the AP from the carotid sinus and aortic arch?

A

cardiovasular centre in the medulla

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19
Q

What pathway will the medulla decrease its activity when bp is high?

A

sympathetic

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20
Q

What pathway will the medulla increase activity when bp is high?

A

parasympathetic nerve

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21
Q

What neurone inhibits the sympathetic pathway when bp is high?

A

inhibitory interneurone

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22
Q

What organ is innervated by 2 nerves in response to a baroreceptor reflex?

A

heart via symp and para nerves

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23
Q

What is the name of the parasympathetic receptor on the heart?

A

M2 AChR

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24
Q

What is the name of the sympathetic receptor on the heart?

A

beta-1 ADR

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25
Q

What 3 other factors are effected by the sympathetic pathway?

A

Arterioles
Veins
Kidney

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26
Q

What receptor doe the sympathetic neurone effect on the 3 other organs/vessels?

A

Arterioles alpha-ADR
Veins alpha-ADR
Kidney beta-ADR

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27
Q

What happens to the heart when baroR detects high BP?

A

decreased CO
release of ACh increased
release of NA decreased

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28
Q

What happens to the arterioles and the veins when the baroR detects high BP?

A

reduces release of NA

relaxation

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29
Q

How does the heart slow down? via parasympathetic neurone

A

ACh released from the post ganglionic fibres of parasympathetic system
Release of ACh to SA node of the atria activates M2AChR
–> slow discharge rate of the AP from SA node = BRADYCARDIA

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30
Q

How does the heart slow down? via sympathetic neurone

A

NorA from post-ganglionic neurone decreases

As NorA increases the frequency of firing AP (beta-1

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31
Q

How does the sympathetic decrease BP via the arterioles?

A

decrease norA, reduces contractile response of norA on arterioles
decrease total peripheral resistance, bp falls

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32
Q

How does the sympathetic neurone decrease BP via the veins?

A

decrease release of NA
decrease alpha-1 ADR stimulation
decrease bp
via frank starling mechanism

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33
Q

How does the sympathetic neurone decrease bp via the kidney?

A

reduce stimulation of beta1 ADR

decrease the release of renin –> decrease bp = vasodilation

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34
Q

What are the important ways which blood flows to the brain and myocardium(heart)?

A 
via carotid arteries at the carotid sinus)
via aorta (aortic arch) respectively
35
Q

What vessels contain the pressure blood pressure sensors in their walls?

A

carotid arteries

aorta

36
Q

What type of receptor is the baroreceptor?

A

mechanoreceptors

sensitive ion channels

37
Q

How do the vessel walls activate the baroR?

A

by stretch not directly by pressure

38
Q

What nerve do carotid afferents travel along?

A

sinus nerve the thence the glossopharyngeal (cranial IX) nerve to the cardiovascular centre in the medulla.

39
Q

What nerve do the aortic arch afferents travel?

A

vagus (cranial X) nerve

40
Q

What are baroreceptors the terminals of?

A

myelinated and unmyelinated sensory fibres that express cation-selective ion channels activated by stretch.

41
Q

What happens when the baroreceptor terminals open?

A

generate a graded receptor potential that causes action potential generation which has both dynamic and static components

42
Q

Why are the baroreceptors specifically located in the aortic arch and carotid sinus?

A

located in key feeder vessels that supply blood to the organs which are essential to survival of the organism

43
Q

What effects the response of the mechanosensitive ion channel?

A

large channel in bp = large change in stretch = large receptor P or depolarisation at the BR terminal

44
Q

What 2 phases can the baroR response be divided into?

A

dynamic and static

45
Q

How can we describe the receptor potential?

A

frequency modulated signal- frequencey of AP discharge in the BR proportional to blood pressure

46
Q

What is the dramatic sustained and maddest sustained pressure figures?

A 
DS= 125 mmHg
MS= 75 mmHg (less firing)
47
Q

What makes up the dynamic component of the arterial bp curve?

A

when systole occurs

48
Q

What make sup the static component of the arterial bp curve?

A

when diastole occurs

49
Q

What can lower the MAP (mean arterial blood pressure) of the blood?

A

when background firing rate of the BR is lower

50
Q

When does BR activity cease?

A

very low pressure (40-60 mmHg)

51
Q

What is RAAS?

A

Renin Angiotensin Aldosterone System

52
Q

What does RAAS play a major role in the regulation of?

A
  • sodium excretion and thus blood volume

- vascular tone directly and indirectly

53
Q

What releases renin?

A

kidney- granule cells of the juxtaglomerular apparatus of the kidney

54
Q

What is renin?

A

a proteolytic enzyme released from granule cells of the juxtaglomerular apparatus of the kidney in response to the above stimuli, and others

55
Q

What activates RAAS?

A

reduction in blood volume and the associated drop in arterial blood pressure

56
Q

Where is renin released to?

A

systemic circulation, acting as a hormone

57
Q

What is renin released in response to?

A

-Renal sympathetic nerve activity (increased)
-Renal perfusion pressure (decreased)
-Glomerular filtration
(decreased)

58
Q

What is angiotensinogen?

A

plasma α2-globulin synthesised and released by the liver

59
Q

What releases angiotensinogen?

A

liver

60
Q

What happens when Renin is released form the kidney and angiotensinogen is released by the liver?

A

enzyme renin coverts angiotensinogen to angiotensin I

61
Q

Where is the enzyme ACE expressed?

A

angiotensin converting enzyme

expressed on the surface of endothelial cells (membrane bound)

62
Q

When does Angiotensin I come into contact with ACE?

A

as blood passes through the pulmonary circulation

63
Q

What does ACE convert Angiotensin I to?

A

Angiotensin II

vasoconstrictor

64
Q

When is renin activated?

A

when blood pressure is low!!

65
Q

What receptor does angiotensin II bind to and activate?

A

AT1receptor (GPCR)

66
Q

How does renin increase [MABP]?

A

Contraction of vascular smooth muscle due to:

  • Activation of smooth muscle AT1 R
  • Increased release of noradrenaline form sympathetic nerves innervating vessels
67
Q

How does renin increase [blood volume and MABP]?

A

1) Cell growth in the heart and arteries
2) Aldosterone
secretion from adrenal cortex –> Tubular Na+
reabsorption and salt retention

68
Q

What does ACE do to Bradykinin?

A

Inactivates bradykinin (vasodilator)

69
Q

What does the effect of ACEIs do to the activation of Bradykinin (potent vasodilator) ?

A

inhibits ACE to covert bradykinin to its inactive form

ACCUMULATES IN THE ALVEOLI CAUSING A COUGH

70
Q

What is an example of a ACEI?

A

Lisinopril

71
Q

What is the effect of Lisinopril?

A

block the conversion of angiotensin I to angiotensin II

72
Q

What 2 molecules can block the effects of renin?

A

Angiotensin Converting Enzyme Inhibitors (ACEIs) and Angiotensin I (AT1) Receptor Blockers (ARBs)

73
Q

What is the effect of ARBs?

A

AT1 receptor antagonists (‘sartans’ e.g. Losartan) – block the agonist action of angiotensin II at AT1 receptors in a competitive manner

74
Q

What is an example of a renin inhibitor not recommended with ARB or an ACEI?

A

ALISKIREN

75
Q

What are the physiological effects of ACEIs?

A
  • Cause venous dilatation (decrease preload) and
  • Arteriolar dilatation (decrease afterload and decrease TPR)
  • ->decreasing arterial blood pressure and cardiac load
76
Q

How do you calculate mean arterial bp?

A

MABP = CP x TPR

77
Q

What is aldosterone?

A

a steroid hormone produced by the adrenal cortex

78
Q

ACEIs cause reduced level of aldosterone’s, what are the effects of this?

A

decrease in circulating levels of aldosterone promotes loss of Na+ and H2O

79
Q

How does ACEIs effect blood pressure? for normal and hypertensive subjects…

A

Cause a small fall in mean arterial blood pressure in normal subjects, much larger effect in hypertensive patients (especially if renin secretion is enhanced – e.g. as a consequence of diuretic therapy)

80
Q

What are the adverse effects of ACEIs?

A
  • May initially cause hypotension – especially in patients also treated with diuretics
  • Dry cough (probably due to accumulation of bradykinin in the lungs)
  • Hyperkalaemia (elevated plasma K+ concentration)
  • Angioedema (painful swelling of tissues involving blood vessels)
81
Q

What is an example of a Angiotensin 1 receptor blocker? (ARBs)

A

Sartans

82
Q

What is the difference between ACEIs and ARBs?

A

ARBs do not inhibit the metabolism of bradykinin

83
Q

What hypotensive drug should people who get a cough from ACEIs use instead?

A

ARBs

84
Q

What are 3 clinical uses of ACE inhibitors and AT1 receptor antagonists? (ACEIs and ARBs)

A
  • HYPERTENSION –>benefit derives from:
    1) reduced TPR and MABP and
    2) possible suppression of proliferation of smooth muscle cells in the media of resistance vessels in the long-term
  • CARDIAC FAILURE –> is associated with inappropriate activation of the RAAS. ACEIs
    1) decrease vascular resistance improving perfusion;
    2) increase excretion of Na+ and H20;
    3) cause regression of left ventricular hypertrophy.

-Following myocardial infection infraction –> cardiac failure

Human Physiology and Pharmacology (31 decks)

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