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Cardiovascular > Unit 1 Day 3 > Flashcards

Unit 1 Day 3 Flashcards

1
Q

inoptropy

A

-contractility or contractile force of heart

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2
Q

lusitropy

A

-relaxation or ability of heart to relax

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3
Q

PKA phosphorylation of L-Type Ca2+ Channels

A
  • GPCR activation
  • slows inactivation
  • inc. entry of trigger Ca2+
  • inc. Ca2+-induced Ca2+ release increases inotropy
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4
Q

PKA phosphorylation of Ryr

A
  • GPCR activation
  • inc. Ca2+ sensitivity
  • inc. inotropy by increasing SR Ca2+ release
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5
Q

PKA phosphorylation of Phospholamban

A
  • GCPR activation
  • relieves inhibition of SERCA
  • faster Ca2+ reuptake into SR
  • inc. lusitropy
  • inc. inotropy by inc. SR Ca2+ load
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6
Q

PKA phosphorylation of Troponin 1

A
  • GPCR activator
  • P-Tn1 decreases Ca2+ sensitivity of troponin C
  • allows faster dissociation of Ca2+ so faster filling = inc. lusitropy (not inotropy)
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7
Q

HCN Channels

A
  • HCN channels produce If current
  • sympathetic regulation of chronotropy
  • norepinephrine binds B adrenergic receptor, activates G protein, activates cAMP, activates HCN channel
  • HCN channel allows net inward (depolarizing) current= If
  • promotes spontaneous action potentials
  • highly expressed in SA node
  • activity inc. by sympathetic stimulation via cAMP binding
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8
Q

L-Type Ca2+ Channels

A
  • norepinephrine binds B adrenergic receptor, activates G protein, activates cAMP, activates PKA, activates L-Type Ca2+ channel
  • net inward (depolarizing) current
  • promotes excitability and spontaneous action potentials
  • activity inc. by sympathetic stimulation
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9
Q

GIRK Channels

A
  • G-protein coupled Inwardly Rectifying K+
  • beta/gamma subunit complex of GPCR can bind GIRK channels
  • parasympathetic regulation of chronotropy
  • primary mechanism for parasympathetic control of heart rate
  • stabilizes Vm near K+ equilibrium potential
  • inc. outward K+ current decreases excitability
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10
Q

Chronotropy

A

heart rate

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11
Q

Vascular Smooth Muscle

A
  • small mononucleate cells
  • no sarcomeres = smooth (NOT STRIATED)
  • no troponin complex, no tropomyosin
  • different contractile mechanism from striated muscle
  • THICK filament regulation
  • Ca2+ enters cytoplasm from SR/plasma
  • Ca2+ binds to Calmodulin
  • Ca2+-CaM binds to myosin light chain kinase to activate it
  • MLCK phosphorylates myosin head- permits cross-bridge cycling
  • myosin light chain phosphatase (MLCP) dephosphorylates MLC and halts contraction
  • cAMP inhibits MLCK-causes VSMC relaxation
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12
Q

a1 adrenergic receptors

A
  • sympathetic stimulation alters vascular tone
  • type of GPCR
  • PKC inc. intracellular Ca2+ and causes vasoconstriction
  • vasoconstriction via IP3 and inc. Ca2+
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13
Q

arterial baroreceptor reflex arc

A
  • stretch of arterial wall activates mechanosensitive eNac Na+ channels on baroreceptor cells
  • low pressure baroreceptors in atria and vena cavae mediate bainbridge reflex (inc. HR in response to stretch)
  • SHORT TERM, rapid negative feedback mechanism for sudden changes in blood pressure
  • inc. in pressure causes inc. in firing of baroreceptors
  • CV control centers dec. sympathetic output and inc. parasympathetic output
  • causes dec in HR and in inotropy
  • in vasculature, dec. tone causes vasodilation
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14
Q

4 tissue metabolites that control local flow to a capillary bed

A
  • primary mechanism to match blood flow in capillaries to metabolic demand
  • adenosine
  • lactic acid
  • CO2
  • K+
  • H+
  • PO4-
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15
Q

Myogenic Response

A
  • autoregulation
  • feedback mechanism to maintain constant flow despite changes in pressure
  • ex. postural changes
  • myogenic response produces vasoconstriction to reduce flow
  • can be overcome by vasoactive metabolites
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16
Q

Nitric Oxide

A

-potent vasodilator
-basal NO release helps set resting vascular tone
-anti-atherogenic- dec. NO associated with greatly inc. risk for atherosclerosis
-NO synthase highly susceptible to CV disease risk factors (smoking)
-NO diffuses across membranes to VSMCs, where it activates guanylate cyclase to produce cGMP
-cGMP activates PKG
-PKG reduces intracellular Ca2+ via activation
of SERCA, and inhibition of L-type Ca2+ channels

17
Q

Endothelin

A
  • vasoconstrictor, produced in vascular endothelium
  • inhibited by NO, ANP
  • binds to ET receptors on VSMC
  • vasoconstriction via IP3 and inc. Ca2+
18
Q

Renin-Angiotensis-Aldosteron System

A
  • primary system for long term control of blood pressure
  • dec mean arterial pressure (hemorrhage) causes inc. renin, causes inc. angtiotensin, causes inc. aldosterone, causes inc. blood volume
  • angiotensin 1 cleaved by angiotensin converting enzyme (ACE) to antiotensin 2 (A2) = vasoconstrictor
19
Q

atrial natriuretic peptide

A
  • vasodilator peptide released by atria
  • released in response to stretch in heart
  • natriuretic = sodium excretion
  • lowers blood pressure
20
Q

The sequence of events during excitation and contraction of cardiac muscle cells is:

A

• Ca2+ enters via DHPR (L-type Ca2+ channel) and activates RyR2 to cause larger
flux of Ca2+ from SR into myoplasm
• Ca2+ activates contraction by binding to troponin on thin filaments.

21
Q

The sequence of events during relaxation of cardiac muscle cells is:

A

• Ca2+ is removed from the myoplasm by:
(i) SERCA2 pump located in longitudinal SR (2 Ca2+ per cycle); Ca2+ diffuses within SR
to terminal cisternae, where it binds to calsequestrin (low affinity, high capacity)
(ii) NCX Na+
/Ca2+ exchanger in junctional domains of plasma membrane and t-tubules.
• SERCA2 dominates since SR surrounds each myofibril; requires less energy since VSR≈0.
• NCX is next in importance and can be arrhythmogenic, as will be discussed later.
• In steady-state, Ca2+ released from SR is recycled back into SR by SERCA2, and surface
extrusion balances L-type Ca2+ current.

22
Q

EC Coupling in Cardiac vs. Skeletal Muscle

A

-Cardiac: requires entry of external Ca2+ DHPR: CaV1.2 (α1C), β2a or β2b, α2δ1, Ca2+ released from SR via RyR2

-Skeletal: does NOT require entry of external Ca2+ DHPR: CaV1.1 (α1S), β1a, α2δ1, γ1
Ca2+ released from SR via RyR1

-Both: Ca2+ binds to troponin on thin filaments and activates contraction

23
Q

NCX Na/Ca Exchanger

A
  • exchanges 2 Na+ for 1 Ca2+
  • can run in either direction, depending on both membrane potential and gradients of Na and Ca
  • sudden inc. Ca could cause cell to Ca to be released from SR and cause cell to depolarize
24
Q

calcium-dependent inactivation

A
  • if amount of Ca in SR inc., great CDI causes less Ca to enter via L-type channel
  • if amount of Ca is dec. then there is less CDI and greater Ca entry via the L type channel
  • helps maintain constant SR Ca contant
25
Q

Stimulation of β-adrenergic Receptors

A

-increases both contraction strength (pos inotropy), and rate of relaxation (pos lusitropy), of cardiac muscle

26
Q

Catecholaminergic Polymorphic Ventricular Tachycardia (CVPT)

A
  • CVPT pts do not display ECG abnormalities at rest but do display them upon exercise or upon infusion of catecholamines
  • mutations in RyR2, that inc. resting leak of Va out of SR or render RyR2 more sensitive to activation of Ca
  • caseuqestirin regulates function of RyR2 and this may also be altered in CVPT
  • CVPT mutations together w/ inc. SR Ca content that is caused by activation of b adrenergic receptors results in releases of Ca
  • occurs shortly or long after repolarization
  • extrusion of this Ca via NCX results in depolarizations that can trigger ectopic action potentials and initiate arrhythmias
27
Q

Timothy Syndrome*

A
  • de novo mutations of the Cav1.2 subunit of the L-type Ca2+ channel result in a lengthened cardiac action potential
  • mutation suppresses voltage-dependent inactivation
  • TS and TS2 pts display AV block, PROLONGED QT INTERVALS, and polymorphic ventricular tachycardia
  • results in syncope, cardiac arrhythmias and sudden death
28
Q

Brugada Syndrome*

A
  • sudden unexplained death syndrome
  • linked to mutations of cardiac Na channel Nav1.5, KChip2, and Cav1.2
  • these mutations cause large reduction in magnitude of L-type Ca current, impairing membrane trafficking
  • these pts have significantly shortened QT interval
29
Q

HFrEF

A

-due to coronary artery disease most commonly

30
Q

HFpEF

A

-due to hypertension most commonly

Cardiovascular (29 decks)

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