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Cardiovascular System > Session 5 - ANS, Control Of BP and Hypertension > Flashcards

Session 5 - ANS, Control Of BP and Hypertension Flashcards

1
Q

What is the neurotransmitter involved in sympathetic preganglionic fibres?

A

Ach

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2
Q

What is the neurotransmitter involved in sympathetic postganglionic fibres?

A

NA

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3
Q

What is the neurotransmitter involved in parasympathetic preganglionic fibres?

A

Ach

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4
Q

What is the neurotransmitter involved in parasympathetic postganglionic fibres?

A

Ach

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5
Q

What is the receptor located on sympathetic preganglionic synapse?

A

Nicotinic Ach receptor

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6
Q

What is the receptor located at sympathetic post ganglionic and target tissue?

A

Adrenoceptor

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7
Q

What is the receptor located on parasympathetic preganglionic synapse?

A

Nicotinic acetylcholine receptor

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8
Q

What is the receptor located on parasympathetic post ganglionic and target tissue?

A

Muscarinic acetylcholine receptor

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9
Q

Where do parasympathetic preganglionic fibres innervating the heart originate from?

A

10th cranial nerve or vagus nerve

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10
Q

Where does preganglionic fibres synapse with postganglionic cells for the heart?

A

Epicardial surface or at SA and AV node

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11
Q

What do parasympathetic postganglionic cells in the heart release?

A

Ach

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12
Q

What kind of receptor does parasympathetic input to the heart use?

A

M2 receptor

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13
Q

What are the 2 effects of parasympathetic input to the heart?

A

Decrease heart rate

Decrease AV node conduction velocity

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14
Q

Where does the sympathetic postganglionic fibres originate from?

A

Sympathetic trunk

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15
Q

Where does the sympathetic fibres innervate in the heart?

A

SA node
AV node
Myocardium

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16
Q

What kind of neurotransmitter does sympathetic postganglionic fibres release?

A

Noradrenaline

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17
Q

What kind of receptors does the sympathetic fibres act on in the heart?

A

Beta 1 adrenoceptor

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18
Q

What are the 2 effects of sympathetic input to the heart?

A

Increase heart rate

Increase force of contraction

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19
Q

How are action potentials in SA node cells fired?

A

Cells in SA node steadily depolarize toward threshold, the depolarizing pacemaker potential as HCN channels open, causing the If funny current
This opens fast Ca2+ channels, causing depolarization
Ca2+ channels close and K+ channels open

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20
Q

How does sympathetic activity affect pacemaker potentials?

A

Sympathetic fibres releases noradrenaline at beta1 receptors, activates Gs unit, stimulating adenylyl cyclase, producing cAMP, which are cyclic nucleotides, opening up more HCM channels and so speeds up pacemaker potential, increasing the slope of the slow depolarization

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21
Q

How does parasympathetic activity affect pacemaker potentials?

A

Parasympathetic fibres release Ach on M2 receptors, which stimulates GI subunit, which inhibits the actions of adenylyl cyclase and decreases cAMP, slowing the opening of HCN channels, and the beta-gamma subunit also increases K+ conductance

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22
Q

How does noradrenaline increase force of contraction?

A

NA acts on beta 1 adrenoceptors in myocardium, causing in increase in cAMP and activation of PKA. PKA phosphorylates Ca2+ channels increasing Ca2+ entry during plateau of action potential and increases uptake of Ca2+ in SR so more can be released, and when more Ca2+ activates tropomyosin, force of contraction is increased

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23
Q

What kind of innervation do most vessels receive?

A

Sympathetic

24
Q

What kind of receptors do most arteries and veins have?

A

Alpha 1 adrenoceptors

25
Q

What kind of receptors do coronary and skeletal muscles vasculatures have?

A

Beta 2 receptors

26
Q

What kind of receptors do circulating adrenaline have higher affinity for?

A

Beta 2

27
Q

At higher concentrations, what other receptor does adrenaline bind to?

A

Alpha 1

28
Q

What is the effect of activating beta 2 receptors?

A

Activates Gs subunit, stimulates adenylyl cyclase, increases cAMP, activates PKA, opens K+ channels, inhibits MLCK, relaxes smooth muscle and so causes vasodilation

29
Q

What is the effect of activating alpha 1 adrenoceptors?

A

Activates Gq subunit, activates PIP2 to be cleaved into IP3, binds to IP3 receptors, increases intracellular Ca2+ from stores and influx of extracellular Ca2+, so contraction of smooth muscle = vasoconstriction

30
Q

What is the baroreceptor reflex?

A

When arterial pressure is increased, the receptors in the carotid sinus and aortic arachnid is stretched, so baroreceptors detects the increase and activates parasympathetic nervous system

31
Q

What is baroreceptor good at?

A

Maintaining blood pressure over short term, compensates for moment to moment changes in BP, but can reset to higher levels with persistent increases in blood pressure

32
Q

What is hypertension?

A

Sustained increase in blood pressure

33
Q

What is normal adult blood pressure range?

A

90/60mmHg to 120/80mmHg

34
Q

What is stage 1 hypertension?

A

More than 140/90mmHg

35
Q

What is stage 2 hypertension?

A

More than 160/100 mmHg

36
Q

What is severe hypertension?

A

More than 180 systolic or more than 110 diastolic

37
Q

What is primary hypertension?

A

Unknown cause of hypertension

38
Q

What is secondary hypertension?

A

Where cause can be defined

39
Q

What is the effect of hypertension?

A

Increase after load, leading to left ventricular hypertrophy, heart failure, and increased myocardial oxygen demand which leads to myocardial ischaemia and MI
Arterial damage can lead to atherosclerosis or weakened vessels, leading to stroke, aneurysms, renal failure or retinopathy

40
Q

What are the 5 organs that can be affected by CVS disease?

A 
Brain 
Heart
Eyes
Arteries
Kidneys
41
Q

What is a form of long term control of blood pressure?

A

Complex interaction of neurohumoral responses to control sodium balance and extracellular fluid volume like plasma

42
Q

What are 4 pathways that control circulating volume and hence BP?

A

Renin-angiotensin-aldosterone system
Sympathetic nervous system
Anti diuretic hormone
Atrial natriuretic peptide

43
Q

What does the renin-angiotensin-aldosterone system do?

A

Renin is released from granular cells of juxtaglomerular apparatus

44
Q

What are 3 factors that stimulate renin release?

A

Reduced NaCl delivery to distal tubule
Reduced perfusion pressure in kidney
Sympathetic stimulation to JGA

45
Q

What is the effect of renin?

A

Renin from juxtaglomerular granule cells catalyze conversion of angiotensinogen to angiotensin I. Then angiotensin converting enzyme (ACE) converts angiotensin I to angiotensin II, which causes vasoconstriction and stimulates Na+ reabsorption at kidney to increase blood pressure, angiotensin II also stimulates aldosterone

46
Q

What is the effect of aldosterone on the kidney?

A

Acts on principal cells of collecting ducts, stimulates Na+ and water reabsorption, activates apical Na+ and K+ channels to increase BP

47
Q

What is the effect of ACE on bradykinin?

A

Angiotensin converting enzyme breaks down vasodilator bradykinin into peptide fragments, hence amplifying vasoconstriction effects of angiotensin II

48
Q

What is the effect of ACE inhibitors?

A

Inhibits ACE, lowers blood pressure

49
Q

What are 4 examples of ACE inhibitors?

A

Captopril
Lisinopril
Perindopril
Enalapril

50
Q

What is the effect of sympathetic nervous system in blood pressure?

A

Decrease Na+ excretion, vasoconstriction, increase BP and stimulates renin release from JG cells

51
Q

What is the effect of antidiuretic hormone on blood pressure?

A

Formation of concentrated urine by retaining water to control plasma osmolarity, increases water reabsorption, causes vasoconstriction, increases blood pressure

52
Q

What is the effect of natriuretic peptides on blood pressure?

A

Promotes Na+ excretion, decreases BP, causes vasodilation

53
Q

What are prostaglandins?

A

Act as vasodilator, enhances glomerular filtration and reduces Na+ reabsorption to decrease BP

54
Q

What is the effect of dopamine on BP?

A

Vasodilation and increases renal blood flow, reduces reabsorption of NaCl, decreases BP

55
Q

How does renovascular disease lead to hypertension?

A

Occlusion of renal artery causes fall in perfusion pressure in kidney, which increases renin production and this activates renin-angiotensin-aldosterone system, and there would be vasoconstriction and Na+ retention in other kidney

56
Q

How does renal parenchyma disease cause hypertension?

A

Direct damage to kidneys causes loss of vasodilator substances, and inadequate glomerular filtration causes Na+ and water retention

57
Q

What are 5 non-pharmacological approaches to treating hypertension?

A 
Exercise
Diet
Reduce Na+ intake 
Reduce alcohol intake 
Lifestyle changes

Cardiovascular System (11 decks)

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