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Cardio > Lecture 23: Vasoactive Mediators > Flashcards

Lecture 23: Vasoactive Mediators Flashcards

1
Q

Describe the effects of Ang II on cardiovascular system

A

Hypertrophy of cardiac myocytes, vascular SM

Inc. EC matrix production by cardiac fibroblasts, vascular SM = remodeling

Proliferation (hyperplasia) of vascular SM

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2
Q

List the Ang II receptors, identifying the major responses mediated by each

A 
AT1 = 
pressor effects (vasoconstriction), CV hypertrophy and remodeling

AT2 =
Vasodilation (NO mediated)
Protective effects on CV structure

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3
Q

Describe synthesis of Ang II

A

Angiotensinogen converted by Renin to

Ang I, which is converted by ACE to

Ang II

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4
Q

What are rapid pressor effects of Ang II?

A

Vasoconstriction
(Directly from AT1
Indirectly from symp.)

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5
Q

What are slow pressor effects from Ang II?

A

Na+ retention, plasma volume expansion
(Directly from AT1 effects on kidneys;
Indirectly with inc. aldosterone production)

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6
Q

What are renin secretion regulators?

A

Sympathetic division

Renal baroreceptors

Macula densa

Hormones

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7
Q

Why is sympathetic division important renin secretion regulator?

A

Major mechanism for increased Ang II when BP falls!

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8
Q

How does sympathetic division regulate renin secretion?

A 
Dec. BP
=
Baroreceptor reflex
=
Inc. symp. Tone to kidneys
=
Stimulation of Beta1 receptors on granular cells
=
Inc. renin secretion
= 
Inc. Ang II = Inc. BP
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9
Q

Where is renin synthesized?

A

Granular cells of kidneys

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10
Q

How do renal baroreceptors regulate renin secretion?

A 
Dec. BP
=
Dec. perfusion pressure
=
Dec. stretch of afferent arterioles in kidney
=
Dec. renin secretion
= 
Inc. Ang. II = Inc. BP
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11
Q

How do hormones regulate renin secretion?

A 
Inc. Ang II 
=
Stimulation of AT1 receptors on granular cells
=
Dec. renin secretion
= 
Dec. Ang II
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12
Q

What are natriuretic effects?

A

Inc. renal excretion of Na+

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13
Q

Where are the natriuretic peptides synthesized and what is their stimulus for release?

A

Synthesized in heart
ANP = atria
BNP = ventricles

Stimulus for release = stretch due to increased pressure or volume

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14
Q

What effects do natriuretic peptides have?

A

Inc. renal extraction of Na

Vasodilation

Protective effects on CV structure

Dec. renin secretion (hormonal renin secretion regulators)

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15
Q

How do NPs and Ang II compare in terms of renin secretion?

A

Both = dec. renin secretion

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16
Q

What can be used as an indicator of LV dysfunction?

A

Increased BNP levels in plasma

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17
Q

How are NPs metabolized?

A

Peptidases =

Neprilysin (NEP)

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18
Q

Describe the use of BNP as a drug

A

Nesiritide = recombinant BNP

Used for acute HF
Vasodilation = dec. BP = dec. AL

Administered IV, limited efficacy

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19
Q

What are NEPi’s?

A

NEP inhibitors

Lead to inc. NPs = vasodilation

Better when combined for less AEs

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20
Q

What are NEPIs usually combined with?

A

NEPIs + ARBs

Sacubitril - Valsartan

= ARNI
(Angiotensin receptor - neprilysin inhibitor)

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21
Q

Describe the synthesis of NO in endothelial cells

A

Synthesized from Arginine

Catalyze by eNOS

22
Q

Identify two mechanisms for activation of endothelial NO synthase (eNOS)

A

1) shear stress on luminal surface of endothelial cell

2) increased intracellular calcium

23
Q

Identify inhibitor of eNOS

A

L-NAME

24
Q

Describe mechanism for NO mediated vasodilation and for termination of this response

A

Increased shear stress on endothelial cells = NO mediated flow induced vasodilation in large arteries in SKM during exercise

25
Q

Describe mechanism for flow mediated vasodilation

A 
Inc. MVO2 
=
Inc. metabolites in myocardial cells
=
Dilation of coronary arterioles
= 
Inc. CBF
=
Inc. shear stress on ECs in surface coronary aa.
= 
Inc. NO synthesis by ECs in surface coronary aa.
=
Dilation of surface coronary aa.
26
Q

Identify at least one example of a mediator that can cause both direct vasoconstriction and NO mediated vasodilation

A

ACh acting at M3 receptors (Gq GPCRs = inc. [Ca]i)

27
Q

Identify two important examples of nitridergic neurotransmission

A

Parasympathetic postganglionic fibers inner sting sphincters in GI, urinary tracts = relaxation

Parasympathetic postganglionic fibers innervating blood vessels in blush areas of face, genital erectile tissue = vasodilation

28
Q

What does nitridergic refer to?

A

Neurons that release NO as a neurotransmitter

29
Q

Describe the vascular effects of the endothelins (ETs)

A

Vasoconstrictors (contribute to basal tone of vascular SM)

30
Q

List the ET receptors, identifying the subtype that mediates most ET effects

A

ETa **

ETb

31
Q

List the drugs that target ET receptors, identifying their major indication

A

Bosentan

Used for PULMONARY HPT

32
Q

List 3 locations of histamine in body, identifying cells that contain majority of the body’s histamine

A

1) GI
2) CNS
3) Mast cells **

33
Q

List important examples of stimuli that trigger release of histamine from mast cells

A

Triple response = localized release

Anaphylaxis = systemic release

34
Q

Identify the major responses mediated by two most important histamine receptor subtypes

A 
H1 = 
Vasoconstriction, bronchoconstriction, inc. GI motility
Activation of eNOS, EC contraction
Pain, itch
Inc. secretion (rhinorrhea)

H2 =
Inc. gastric acid secretion
Vasodilation

35
Q

Describe histamine vascular effects

A

Vasoconstrictor (veins, venules) from direct stimulation of H1

Vasodilator (from NO mediated and direct stimulation of H2)

Inc. vascular permeability from EC contraction

36
Q

Describe the triple response that follows local release of histamine from mast cells under skin

A 
Erythema
NO mediated (H1) + direct H2 vasodilation

Flare
Stimulation of H1 sensory fibers leads to release of vasodilator neuropeptides

Wheal
Arteriolar dilation (NO + direct H2)
Venoconstriction (H1)
Contraction of ECs

37
Q

Describe the synthesis of kinins and explain why the term kallikrein-kinin system (KKS) is used when discussing the kinins

A

Kininogens are converted to kinins by kallikreins

Rate of kallikrein synthesis and/or activation = main determinant of rate of BK synthesis

38
Q

What is bradykinin (BK) metabolized by?

A

ACE

39
Q

Where is kallikrein released from?

A

Mast cells!

40
Q

What are the vascular effects of kinins?

A

Vasoconstrictors (veins, venules)

Vasodilators (NO mediated)

Inc. vascular permeability from EC contraction

41
Q

Describe effects of kinins on the respiratory system

A

Bronchoconstriction, cough

42
Q

Identify the major indication for drugs that are used to antagonize the KKS

A

Hereditary angioedema (caused by high levels of kinins)

43
Q

Define eicosanoid and list two major classes

A

Derived from membrane phospholipids, with arachidonic acid important FA precursor

Prostanoids (from COX)
Leukotrienes (from LOX)

44
Q

What are important examples of prostanoids?

A

Prostanoids =
TXA2 (thromboxane)
PGI2 (prostacyclin)

45
Q

What are vascular effects of PGI2 and TXA2? PGE2?

A

PGI2 = vasodilation,
Dec. platelet aggregation

TXA2 = vasoconstriction,
Inc. platelet aggregation

PGE2 = vasodilation

46
Q

Where do eicosanoids produce physiological effects?

A

Bronchial SM

GI secretions

Kidneys

Inflammation, pain, fever

47
Q

What are physiological effects of eicosanoids?

A

bronchial SM
PGE2, PGI2 = dilation
Leukotrienes = constriction

GI secretions
PGE2, PGI2 = dec. acid, more mucus, bicarbonate

Kidneys
PGs = vasodilation = inc. renal blood flow = inc. glomerular filtration

48
Q

Describe major indications of PGs and synthetic analogs that have effects on vasculature

A

Epoprostenol, nIloprost, Treprostinil
Synthetic PGI2 for pulmonary HPT

Alprostadil
Synthetic PGE1 for maintenance of ducts in neonate with congenital heart disease

49
Q

Identify the most important category of eicosanoid antagonists

A

NSAIDs block COX = dec. prostanoids

50
Q

List primary adverse effects of NSAIDs

A

GI - abdominal pain, peptic ulcers, bleeding

Kidneys = dec. renal blood flow, glomerular filtration (from less vasodilator PGs)

Inc. risk of CV thrombotic events = MI, stroke (dec. PGI2 = inc. platelet agg)

Prolonged bleeding (dec. synthesis of TXA2)

Premature closure of ductus arteriosus in fetus

Cardio (8 decks)

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