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PHARM 203 (Final) > Vasoactive (General) > Flashcards

Vasoactive (General) Flashcards

1
Q

Why is it important to maintain proper blood pressure

A

Sympathetic System ensures all organs get proper blood flow

Helps regulate body temperature

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2
Q

Cardiac Preload

A

Initial stretching that occurs during ventricular filling

Higher Preload = Higher Afterload

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3
Q

Cardiac Afterload

A

Pressure that heart has to pump against and overcome

Greater Pressure = Greater Load, Heart has to pump harder

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4
Q

Capacitance Vessels

A

Venous System:
- Stores blood
- Most blood is stored in venous system
- Stored blood can be recruited when needed

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5
Q

Resistance Vessels

A

Arterial System
- Lots of control
- Provides resistance to blood flow

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6
Q

Vascular Tone
- What parts of vascular system have muscles
- What kind of muscle is this?
- What is the function of these muscles?

A

Wall of arteries, arterioles, venules, veins all contain smooth muscle
- Less smooth muscles in veins

Controls vasodilation/vasoconstriction

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7
Q

What controls Vascular Tone

A

Endothelium
Circulating Hormone
Sympathetic Nerve

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8
Q

How is Vascular Tone controlled

A

Ca2+ regulates vascular smooth muscle cells
- Vascular SM contracts when Ca2+ rises
–> Vasoconstriction

  • Vascular SM relax when Ca2+ decreases
    –> Vasodilation
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9
Q

Process of Muscle Contraction

A
  1. Ca2+ rises, forms complex if Calmodulin
  2. Complex activates Myosin Light Chain Kinase (MLCK)
  3. MLCK phosphorylates myosin
  4. Myosin can now crossbridge with actin
  5. Initiates contraction
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10
Q

Process of Muscle Relaxation

A

Myosin Light Chain Phosphatase (MLCP) dephosphorylates MLC leading to relaxation
–> Inhibition of MLCP maintains contraction

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11
Q

Methods Agents use to Cause Contraction

A

Increase Ca2+:
- Release intracellular Ca2+ via IP3
- Depolarizing membrane and opening voltage-gated Ca2+ channels
–> Allow Ca2+ entry intro cell

MLCK/MLCP Activity:
- Increase MLCK activity
- Decrease MLCP activity

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12
Q

Methods Agents use to Cause Relaxation

A

Decrease Ca2+:
- Hyperpolarize membrane (Open K+ Channels)
- Inhibit Ca2+ entry by blocking VGCC

cGMP/cAMP rise –> Vascular Smooth Muscle Relaxation:
- Increase Intracellular cAMP
–> Activates MLCP & promote Ca2+ efflux
- Increase intracellular cGMP
–> Activates MLCP & opposes agonist induced Ca2+ increase

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13
Q

Vascular Tone (Endothelium)

A

Produces Vasodilators and Vasoconstrictors
- Also important for platelet regulation

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14
Q

Vascular Tone (Endothelium)
- Vasodilation

A

Major Vasodilators Produced by Endothelial Cells

Nitric Oxide (EDRF = Endothelial Relief Factor)

Prostanoids (PGI2)

Endothelial-Derived Hyperpolarizing Factor (EDHF)
–> Most likely Ca2+ activated K+ Channels that cause hyperpolarization of Endothelium which spreads to smooth muscles

C-Natriuretic Peptide (CNP)
–> Increase cGMP

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15
Q

Vascular Tone (Endothelium)
- Vasoconstrictor

A

Major Vasoconstrictors Produced by Endothelial Cells

Endothelin
Thromboxane A2 (Platelets)
Angiotensin II

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16
Q

Endotheline (ET)
- Produced by?
- Hormone or Local Mediator

A

Endothelial Cells

Acts as a local mediator

17
Q

Endotheline (ET)
- Mechanism of Action
- Effect

A

Binds ET(A) Receptors expressed by Vascular Smooth Muscle Cells

Causes vasoconstriction by IP3-mediated Ca2+ release

18
Q

Vascular Tone (Circulating Hormones)
- What are the different methods hormones control vascular tone?

A

1 Renin-Angiotensin System (RAS)

  1. Antidiuretic Hormone (ADH/Vasopressin)
  2. Bradykinin
19
Q

Renin-Angiotensin System (RAS)
- Overall Effect

A

Vasoconstriction
- Aldosterone stimulates salt/water reabsorption by kidney

20
Q

Renin-Angiotensin System (RAS)
- Entire Process

A
  1. Renin is secreted by Kidney
  2. Renin cleaves Angiotensinogen into Angiotensin I
  3. Angiotensin-Converting Enzyme cleaves Angiotensin I into Angiotensin II
  4. Ang II Binds AT1 receptors on SMC resulting in vasoconstriction
21
Q

Antidiuretic Hormone (ADH/Vasopressin)
- Released by?
- Effect

A

Secreted by posterior pituitary

Causes vasoconstriction by:
- Binding V1 Receptors on Smooth Muscle Cells
- Water retention

22
Q

Bradykinin
- Released by
- Effect

A

Generated from Kininogen by Kallikrein

Mediates vasodilation by endothelial NO generation

23
Q

What does ACE do

A

Cleaves Angiotensin I to Angiotensin II

Cleaves and inactivates vasodilator bradykinin

24
Q

Vascular Tone (Sympathetic Nerves)
- Regulates what?

A

Regulates arterial, arteriole, venous, vein diameter

25
Q

Vascular Tone (Sympathetic Nerves)
- Stimulation

A

Sympathetic Nerve stimulation releases norepinephrine (NE)
- Effects are Vascular System Dependent

26
Q

Vascular Tone (Sympathetic Nerves)
- NE acts on Alpha-1 Smooth Muscle Cells

A

Induces Vasoconstriction
- Ex. BP regulating resistance arteries

27
Q

Vascular Tone (Sympathetic Nerves)
- NE acts on Beta-2 Endothelial Cells

A

Induces Vasodilation
- Ex. Blood vessels of skeletal muscles

PHARM 203 (Final) (41 decks)

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