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Pharm Block 2 > 11 - Smooth Muscle Pharmacology > Flashcards

11 - Smooth Muscle Pharmacology Flashcards

1
Q

What facilitates smooth muscle contraction? What causing contraction in vascular smooth muscle?

A

Electrochemical coupling operates through changes inc cell membrane potential.

Resting membrane potential = -40 to -70 mV.

K channels cause hyperpolarization while calcium channels cause depolarization.

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2
Q

What is pharmacological coupling of smooth muscle? What else can cause smooth muscle contraction?

A

Operates independent of cell membrane potential.

Involves receptors, intracellular signaling.

Nts, hormones, and paracrine factors.

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3
Q

What is the main mechanism of smooth muscle contraction? What causes relaxation?

A

Ca2+ channels allow calcium into cells and sarcoplasmic reticulum releases Ca2+.

Ca binds to calmodulin activating MLC kinase, which phosphorylated actin+MLC and causes contraction.

When RoA is bound to GDP it’s inactive and Rho kinase is inactive. As a result, myosin phosphatase is UN-phosphorylated and can remove a phosphate from MLC to cause muscle relaxation.

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4
Q

What are three mechanisms of smooth muscle relaxation?

A

Blocking calcium channels, blocking Galpha receptors, and blocking Rho kinase.

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5
Q

What are the different parts of the body that can be targeted by smooth muscle relaxation?

A

CV - vasodilators
Obstetrics - uterine relaxation
GI motility - contraction
Pulmonary - bronchodilators

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6
Q

What is preload? When is it increased?

A

The volume of blood in the ventricles at the end of diastole (end diastolic pressure).

Increased in hypervolemia and regurgitation of cardiac valves.

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7
Q

What is afterload? When is it increased?

A

Resistance that the left ventricle must overcome to circulate blood.

Increased in HTN and vasoconstriction.

Increased afterload = increased cardiac workload

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8
Q

What are five pharmacological actions of vasodilators?

A
  1. Nitric oxide
  2. Increase or decrease cell membrane channel activity (K+ or Ca2+ channels)
  3. Increase smooth muscle cell cAMP or cGMP levels
  4. Activate vasodilator receptors
  5. Inhibit vasoconstrictor pathways and receptors
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9
Q

What are the types of nitric oxide donors? How does their mechanism of action differ?

A

Organic Nitrates - indirectly increase through S-nitrosothiol

Sodium Nitroprusside - direct NO donor

Both work to increase cGMP and protein kinase G.

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10
Q

What drug is an organic nitrate that that acts on venous circulation? What is it used for and how is it given? What is the toxicity?

A

Nitroglycerin

Sublingual - works within 15-30 min. Treats angina/coronary artery disease.

Toxicity is hypotension and reflex tachycardia.

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11
Q

What drug is a NO donor that works on both arterial and venous circulation? When is it used? How is it given? What is the toxicity?

A

Nitroprusside - direct NO donor.

IV for HTN emergencies for rapid reduction in art pressure. Lasts 15-30 min.

Toxicity: hypotension, cyanide accumulation (needs monitoring).

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12
Q

What is a direct vasodilator that acts on arterial circulation and is used in heart failure and HTN? How is it given?

A

Hydralazine

Oral for long-term, combined with nitrates for heart failure.

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13
Q

What direct vasodilator works on arterial circulation and is a selective K+ ATP channels opener? What is it used for and how is it given? What is the side effect?

A

Minoxidil.

Used for heart failure and HTN.

Oral for long-term.

Hypertrichosis (hair growth–ROGAIN).

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14
Q

What direct vasodilator acts on arterial circulation and is a non-selective K+ channel opening? When is it used? How is it given? What is the toxicity?

A

Diazoxide.

Used in HTN emergencies.

Oral is long acting, IV for rapid decrease in vascular resistance and art BP.

Toxicity is hypotension.

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15
Q

What are the three types of membrane channel dilators (Ca2+ channel blockers)? What drugs fall into each category?

A

Phenylalkamines - verapamil

Benzothiazapines - diltiazem

Dihydropyridines - nifedipine, nicardipine, amlodipine

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16
Q

Where is the action of calcium channel blockers? Which ones are more vascular smooth muscle selective and which is cerebral vascular selective?

A

They are arterial dominant.

Vascular smooth muscle selective: dihydropyridines

Cerebral vascular selective: Nimodipine

17
Q

What is the use of calcium channel blockers?

A

HTN, angina, cerebral and coronary vasospasm.

18
Q

Which phosphodiesterases are present in vascular smooth muscle? What is the result of inhibiting each?

A

PDE5: inhibition causes increase in cGMP and causes vasodilation via PKG.

PDE3: inhibition causes an increase in cAMP and PKA, resulting in relaxation

Both of these cause smooth muscle relaxation.

19
Q

Which phosphodiesterase is present in the heart? What is the result of inhibiting it?

A

PDE3: inhibition causes an increase in cAMP and enhances the contraction of the heart. Also decreases afterload.

20
Q

Which phosphodiesterase inhibitors cause PDE3 inhibition? What effect do they have on the heart and vascular smooth muscle?

A

Milrinone and Inamrinone

Heart: causes increased force and velocity of contraction

Vascular smooth muscle: dilation of arterial side

Both work through an increase in cAMP.

21
Q

What is the use of PDE3 inhibitors such as Milrinon and Inamrinone? How are they given?

A

Heart failure.

IV for short-term life-threatening heart failure.

Oral forms withdrawn due to sudden cardiac death.

22
Q

Which drugs are PDE5 inhibitors? What is their action and use?

A

Sildenafil and tadalafil

PDE5 inhibition through an increase in cGMP.

Erectile dysfunction and pulmonary HTN.

23
Q

What miscellaneous vasodilator acts as a dopamine D1 agonist? Where is it’s site of action? What is it used for?

A

Fenoldopam

Arterial dominant, natriuretic.

Used in HTN emergencies and post-operative HTN (IV).

24
Q

What miscellaneous vasodilator is an alpha-adrenergic blocker? What is it’s site of action?

A

Prazosin

Arterial and venous circulation.

Used for HTN.

First dose phenomenon.

25
Q

What drug is an oxytocin receptor antagonist that decreases the frequency of uterine contractions?

A

Atosiban

Used to inhibit uterine contractions and prevent preterm labor.

26
Q

What drugs are PGE1 analogs? What is their use?

A

Misoprostal: oral/sublingual to stimulate uterine contractions and prevent/treat postpartum hemorrhage.

Alprostadil: smooth muscle relaxing to maintain ductus arteriosus in neonates b4 card surgery. Erectile dysfunction.

27
Q

What are two labor-inducing drugs? What do they do?

A

Oxytocin: causes uterine contractions

Ergonovine: ergot alkaloid rye fungi. Small doses cause rhythmic uterine contractions ; large doses cause powerful prolonged uterine contractions.

28
Q

What drug is a dopamine D2 receptor antagonist that allows for increased cholinergic smooth muscle stimulation (GI motility)? What are its uses?

A

Metoclopramide.

Treats gastroesophageal reflux disease (GERD), prevents/treats emesis, and impaired gastric emptying.

29
Q

What muscarinic receptor agonist increases GI and bladder contractions? What is its therapeutic use?

A

Bethanechol.

Used for diabetic neuropathy pts with GI and urinary motility problems.

30
Q

What drug can be used to stimulate motilin receptors on GI smooth muscles to promote migrating motor complexes? What are it’s therapeutic uses?

A

Erythromycin - a macrolide antibiotic.

Given IV for gastroparesis and to promote gastric emptying for endoscopy.

31
Q

What are the drugs that are B2 adrenergic agonists? What is their action?

A

Albuterol, Pirbuterol, Terbutaline, Salmeterol, and Formoterol

Bronchodilation through a decreased Ca2+ and K+ channel acvitation.

32
Q

What are the uses of B2 adrenergic agonists? What is the associated toxicity?

A

Inhaled and long acting for asthma and COPD.

Terbutaline inhibits uterine contractions with premature labor.

Can cause tachycardia due to it’s B2 stimulation.

33
Q

What drugs are muscarinic receptor antagonists that inhibit airway smooth muscle contraction and inhibit mucus secretion? What are they used to treat?

A

Ipratropium and Tiotropium.

Inhaled and long-acting for asthma and COPD.

34
Q

Which bronchodilators act through PDE3 inhibition and adenosine receptor antagonism? What are their therapeutic uses? How are they given?

A

Theophylline and aminophylline.

Orally for asthma and COPD.

35
Q

What are three endothelial factors that influence smooth muscle tone? Which receptor does each act on and what is the result?

A

Prostacyclin (PGI2) and IP receptor: increase contraction and prolif.

Endothelin-1 and ETA receptor: Vasodilation

NO and sGC (soluble guanylate cyclase) receptor: cGMP increases for vasodilation

36
Q

What occurs with the IP receptor, ETA receptor, and sGC receptor in pulmonary HTN?

A

Increased endothilin-1 binds ETA receptor to cause increased contraction and proliferation.

PGI2 and NO are reduced, resulting in reduced vasodilation.

37
Q

What drugs are PGI2 (IP) receptor agonists that are used for pulmonary HTN? How are they given?

A

Epoprostenol and Iloprost

Given IV or inhaled. Short half life of 15-30 min.

Lowers peripheral, pulm, and coronary vascular resistance.

38
Q

What drugs are ETA receptor antagonists that treat pulmonary HTN? How is this drug given?

A

Bosentan and Ambrisentan

Lowers pulmonary resistance in pulmonary arterial HTN.

Given orally, IV, or inhaled

39
Q

What drug can be used for pulmonary HTN, acute hypoxemia, and cardiopulmonary resuscitation? What is it’s mechanism of action?

A

Nitric Oxide.

Reduces pulmonary artery pressure and improves perfusion to ventilated areas.

Inhaled.

Pharm Block 2 (12 decks)

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