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PDA Block 2 > Smooth Muscle Physiology > Flashcards

Smooth Muscle Physiology Flashcards

1
Q

What is resting membrane potential

A

-40 to -70mV

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2
Q

contraction occurs when membrane potential is

A

more positive (depolarized)

*Ca rushes in

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3
Q

relaxation occurs when membrane potential is

A

more negative (hyperpolarized)

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4
Q

describe smooth muscle contraction

A

agonist binds to gq receptor which activates PLC which converts PIP2 to DAG and IP3 which causes release of Ca from the sarcoplasmic reticulum.

Also Ca rushed in through voltage gated Ca channels.

Then Ca/Calmodulin is activated which activates MLC Kinase.

MLC kinase phosphorylates MLC which causes contracteion.

Active Myosin phosphatase dephsphorylates MLC making MLC relax.

Myosin phosphatase was activated which RhA-GDP (inactive) was converted to RhoA-GTP and then dephosphorylated myosin phosphatase activating it

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5
Q

Mechanisms of smooth muscle contractin

A
  • pharmacological coupling
  • receptors/Intracellular signaling
  • neurotransmitters, hormones, paracrine factors
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6
Q

Mechanisms of smooth muscle relaxation

A

paracrine factors

membrane potential

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7
Q 
Therapeutic Application for smooth muscle relaxation
CV
Obstetrics
GI Motility
Pulmonary
A
  • CV:vasodilators
  • OB: uterin relaxation
  • GI Motility: contraction
  • Pulmonary: bronchodilators
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8
Q

Preload

A

volume of blood in the ventricles at the end of diastole (EDP)

-increase in: hypervolemia, regurgitation of cardiac valves

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9
Q

Afterload

A

Resistance left ventricle must overcome to circulate blood

  • increased in hypertension, vasoconstriction
  • increase in after load causes and increase in cardiac work load
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10
Q

Pharmacological Actions of Vasodilator drugs

A
  • NO
  • Increase or decrease cell memebrane channela ctivity
  • increase smooth muscle cAMP or cGMP levels
  • activate vasodilator receptors
  • inhibit vasoconstrictor pathways and receptors
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11
Q

Nitric Oxide donors mechanism of action is via which second messengers

A

-cGMP and protein kinase G

Nitric oxide combines with the heme group of soluble guanylyl cyclase (sGC),
activating that enzyme and causing an increase in cGMP. An increased smooth
muscle cGMP level activates K+ channels and enhances myosin light chain (MLC)
dephosphorylation to cause relaxation.

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12
Q

Nitroprusside

A

arteriole and venule dilator

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13
Q

Organic Nitrates

A
  • Nitroglycerin

- Nitroprusside

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14
Q

Nitroglycerin

A

Action: Venous Circulation (dominant) (decrease preload)

Use: Angina/ Coronary Artery Disease

Administration: Sublingual to avoid first pass effect. Reaches therapeutic levels quickly and has short duration (15-30 minutes)

Contraindication: Elevated intracranial pressure

Toxicity: Hypotension, tachycardia

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15
Q

Nitropruside

A

Action: NO releasing
Arterial and Venous circulations (decrease afterload and decrease preload)

Use: Hypertensive emergencies-rapid reduction in arterial pressure

Administration:
Intravenus
Rapid offset after discontinuing
Short duration (15-30 minutes)

Toxicity:
Hypotension, cyanide accumulation

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16
Q

Direct Vasodilators

A

Hydralazine
Minoxidil
Diazoxide

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17
Q

Hydralazine

A

Action: ***Arterial circulation (decrease afterload)

Use: Heart failure/HTN

Administration: oral for long term , combined with nitrates for heart failure

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18
Q

Minoxidil

A

Action: ***Arterial circulation decrease afterload, adn K ATP CHannel opener

Use: Heart failure/ Hypertension

Administration: oral for long-term

Toxicity: Hypertrichosis (hair growth)

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19
Q

Diazoxide

A

Action: Arterial circulation (decrease afterload)
K channel opener

Use: Hypertensive emergencies

administration:
oral-long acting
IV-rapid decrease in vascular resistance and arterial blood pressure

Toxicity: Hypotension

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20
Q

Ca Channel blockers

A
  1. Dihydropyridines-nifedipine, nicardipine, amplodipine
  2. Phenylalkylamine-Verapamil
  3. Benzothiazapines-dilitazem
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21
Q

Calcium channel blockers infor

A

Action: ***Arterial circulation (dominant), Vascular smooth muscle selectivity-dihydropridines are greater ration vascular versus cardiac effects.
Nimodipine has cerebral vascular selectivity

Use: HTN
Angina
Cerebral and coronary vasospasm

22
Q

Phosphodiesterase Inhibitors what are the effects of the different phosphodiesterases on the vascular smooth muscle vs. the heart

A

VSM:
1.cGMP causes relaxation and is broken down by PDE5. So a PDE5 inhibitor would increase cGMP

  1. cAMP causes relaxation and is broken down by PDE3. so a PDE3 inhibitor would increase cAMP

Heart
1. Only cAMP is active. and is broken down by PDE3. SO a PDE3 inhibitor would increase cAMP which would increase contractility bc in the heart cAMP increases contractility

23
Q

Wht is the differenc ebetween what cAMP does in the VSM vs in the heart

A

cAMP in the VSM causes relaxation and therefore vasodilation,

cAMP in the heart causes an increase in contractility

24
Q

PDE3 Inhibitors

A

Milrinone, Inamrinone

heart
*phosphorylation of Ca Channels-inotropic

*Phosphorylates microfilaments-Inotropic

Phosphorylates K Channels and repolarizes-Chronotropic

VSM:
Inhibits myosin light chain kinase
phosphorylates K channels-hyperpolarization

25
Q

Milrinone, Inamrinone

A

Action: PDE3 inhibition increases cAMP

Use: heart failure

Administration: *IV-short term life threatening heart failure
*oral forms were withdrawn due to sudden cardiac death

26
Q

PDE5 Inhibitors

A

Sildenafil, Tadalafi

27
Q

Sildenafil, Tadalafi

A

Action: PDe5 inhibition increases cGMP

Use: erectile dysfunction, pulmonary hypertension

28
Q

Miscellaneous vasodilators

A

Fenoldopam

Prazosin

29
Q

Fenoldopam

A

Action: Dopamine D1 receptor agonist, **Arterial dominant, Natriuretic

Use: Hypertensive emergencies, Post-operative hypertension (IV)

30
Q

Prazosin

A

Action: Alpha adrenergic blocker (a1), **Arterial and venous circulations

use: hypertension

31
Q

Tocolytic drugs

32
Q

Atosiban

A

nonapeptide oxytocin receptor antagonist to decrease frequency of uterine contractions,

Use: Inhibit uterine contractions-prevent preterm labor

33
Q

PGE1 Analogs

A

Misoprostol and Alprostadil

34
Q

Misoprostol

A

oral or sublingual stimulate uterin contractions/prevent treat postpartum hemorrhage (btw we learned this as a side effect in the last lecture and elarned that is main use is to decrease gastric acid secretions)

35
Q

Alprostadil

A

smooth muscle relaxing to maintain ductus arteriosus patent in neonates awaiting cardiac surgery, and erectile dysfunction

36
Q

Labor inducing drugs

A

Oxytocin

Ergonovine

37
Q

Oxytcin

A

uterine contractions

38
Q

Ergonovine

A

Ergot alkaloid rye fungi
-small doses-evoke rhythmic contractions of uterus

high doses-powerful and prolonged uterine contractions

39
Q

Gastrointestinal Motility

A

Metoclopramide

40
Q

Metoclopramide

A

Action: Dopamine D2 receptor antagonist allows for increased cholinergic smooth muscle stimulation

use: GERD, prevent or treat emesis, impaired gastric emptying

41
Q

bethanechol

A

muscarinic receptor agonist

  • increases gastrointestinal and bladder contractions
  • does not cross blood brain barrier
  • not hydrolyzed by cholinesterase-long duration

-use: Diabetic neuropathy patients with GI and urinary motility problems

42
Q

Erythtomycin

A
  • Action: Macrolide antibiotic, stimulates motilin receptors on GI smooth muscl to promote migrating motor complexes (increase gastric emptying)
    use: intravenous gastroparesis (tolerance), acute upper GI hemorrhage to promote gastric emptying for endoscopy
43
Q

Bronchodilators

-B2 Adrenergic Agonists

A

Albuterol, Pirbuterol, Terbutaline, Salmeterol, Formoterol

44
Q

Albuterol, Pirbuterol, Terbutaline, Salmeterol, Formoterol

A

Action: B2 receptor agonists- smooth muscle decrease calcium and K channel activation, bronchodilation, prevent microvascular leakage and bronchial mucosal edema, increase mucous clearance

use: Asthma and COPD
terbutaline-inhibit uterine contractions with premature labor

Administration-inhaled long acting

Toxicity: TACHYCARDIA (bc there are B2 receptors in the heart that function to increase heart rate

45
Q

Bronchodilators – Anti-Cholinergic

A

Ipratropium, Tiotropium

46
Q

Ipratropium, Tiotropium

A

Action: Muscarini receptor antagonists-inhibit airway smooth muscle contraction, inhibits mucous secretions

use: Asthma and COPD

Administration: inhaled long acting

47
Q

Bronchodilators

A

Methylxanthine, Theophylline, Aminophylline

48
Q

Methylxanthine, Theophylline, Aminophylline

A

Action: PDE inhibition, Adenosine receptor antagonism, anti-inflammatory

Use: Asthma and COPD

Administration: oral

49
Q

Pulmonary HTN

A
  • Prostacyclin (PGI2) and the IP receptor
  • Endothelin-1 and ETA receptor
  • Nitric xide and sGC
50
Q

Epoprostenol, Iloprost

A

Action: PGI2 (IP) receptor agonists- lowers peripheral, pulmoary and coronary vascular resistance

use: pulmonary hypertension

Administration: IV and Inhalation, short half lives (5-30 min)

51
Q

Bosentan, Ambrisentan

A

Action: ETA receptor Antagonists- lowers pulmonary resistance in PAH

Use: Pulmonary HTN

Administration:
Oral IV and inhalation

52
Q

Nitric Oxide and Pulmonary HTN

A

Action: Reduces pulmonary artery pressure, improves perfusion to ventilated areas

Use: Pulmonary HTN, Acute hypoxemia, Cardiopulmonary resuscitation

Administration: Inhalation

PDA Block 2 (13 decks)

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