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Pharmacology > Smooth Muscle > Flashcards

Smooth Muscle Flashcards

1
Q

Nitric Oxide Donors Mechanism of Action

A

CGMP/ Protein Kinase G–> Nitrates are metabolized by mtALDH2 to make NO which combines with heme group of guanylyl cyclase to activate the enzyme and increases cGMP levels which then activates protein kinase G and activates K channels and enhances MLC de phosphorylation and interferes with vasoconstriction

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2
Q

Nitroglycerin

A

Organic nitrate
Action: venous circulation (preload)
Use: angina/ coronary artery disease
Administration: sublingual to avoid first pass effect and reaches therapeutic levels quickly with a short duration of action
Contraindication: elevated intracranial pressure
Toxicity: hypotension, tachycardia, syncope, throbbing headache
Tolerance can develop with long acting preparations (oral and transdermal) or continuous intravenous infusions
Metabolism: by mt ALDH in venous smooth muscle

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3
Q

Nitrorpusside

A

Organic Nitric Oxide donor
Relaxation of arterial and venous ciruclation (mainly arterial)–> decrease preload and afterload so SV increases
Complex of iron, cyanide and nitroso moiety
Rapidly metabolized by uptake into RBC with release of NO and cyanide
Sodium nitrorpusside breaks down to generate 5 cyanide molecules and a single NO and cyanide is metabolized by mt rhodanese to thiocyanate
Rapid reduction in arterial pressure–> intravenous infusion lowers BP and the effect disappears 10 minutes after discontinuation
Sensitive to light
Tolerance does not occur
Toxicity- hypotension, cyanide accumulation, metabolic acidosis, arrhythmias

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4
Q

Hydralazine

A

Direct Vasodilator
Arterial circulation (dominant)
Uses: heart failure and hypertension
Administration: oral for long term, combined with nitrates for heart failure (esp. If both hypertension and HF)
Toxicity: headache, nausea, anorexia, palpitations, sweating, and flushing

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5
Q

Minoxidil

A

Direct Channel Dilators
Arterial circulation
Uses: active metabolic activates K channels in smooth muscle membranes resulting in hyperpolarization
Treat Heart failure and hypertension
Toxicity: fluid and salt retention, CV effects and hypertrichosis

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6
Q

Diazoxide

A

Direct Channel Vasodilator
Arterial circulation
Mechanism of Action: activate potassium channel in smooth muscle membranes resulting in hyperpolarization
Long acting parenterally administer
Rapid fall in systemic vascular resistance and mean arterial blood pressure after injection
Hypertensive emergencies and hypoglycemia secondary to insuling a
Toxicity: hypotension and hyperglycemia

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7
Q

Ca Channel Blockers

A

Dihydropyridines: nifedipine, nicardipine, amlodipine
Phenylalkylamine: verapamil
Benzodiazepines: diltiazem

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8
Q

Ca Channel Blockers

A

Vascular Smooth Muscle selectivity- Dihydropyridines greater ratio of vascular smooth muscle effect relative to cardiac effects compared to other two groups and Dihydropyridines have different potency in different vascular bed. Nimodipine is selective for cerebral blood vessels
Arterial Circulation
Hypertension, Angina, Cerebral, Coronary Vasospasm–> reduce cerebral damage after thromboembolic stroke
Toxicity: cardiac-bradycardia, AV block, cardiac arrest, heart arrest
Other-flushing, dizziness, nausea, constipation (verapamil), peripheral edema

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9
Q

Nimodipine

A

has high affinity for cerebral blood vessels and reduces morbidity after subarachnoid hemorrhage

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10
Q

Nicardipine

A

Used by intravenous and intracerebral arterial infusion to prevent cerebral Vasospasm associated with stroke

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11
Q

Verapamil

A

Lacks cerebral vascular selectivity and can be administer intrarterially for stroke

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12
Q

Milrinone, Inamrinone

A

Phosphodiesterase 3 Inhibitors
PDE3 inhibition causes increases in cAMP and PKA phosphorylation which activates cardiac Ca channels and vascular smooth muscle K channels–> increased contraction in cardiac but vasodilation in vascular smooth muscle.
Positive cardiac ionotropic and vasodilator actions
Heart Failure–> intravenous for short term treatment of life threatening treatment of heart failure
Contraindication: cilostazol (oral) is contraindicated in heart failure
Toxicity: arrhythmia, headache, thrombocytopenia

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13
Q

Sildenafil, Tadalafil

A

PDE5 inhibition increases cGMP
Use: erectile dysfunction, pulmonary hypertension
Relax non vascular smooth muscle of the corpa cavernosa to cause erection
Toxicity: adverse side effects with nitrates
Sildeanafil- color vision

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14
Q

Fenoldopam

A

Miscellaneous Vasodilators
Dopamine D1 receptor agonist resulting in dilation of peripheral arteries and natriuresis
Hypertensive emergencies and postoperative hypertension
Intravenous
Toxicity: reflex tachycardia, headache, and flushing
Increase intraocular pressure and should be avoided in patients with glaucoma

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15
Q

Prazosin

A

Alpha adrenergic blocker
Arterial and venous circulation (block a1 receptors in arterioles and venules)
Hypertension
Toxicity: reflex tachycardia, dizziness, and headache
First dose effect

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16
Q

Uterine Smooth Muscle

A 
Atosiban
Misoprostol
Aprostadil
Oxytocin 
Ergonovine
17
Q

Atosiban

A

Oxytocin receptor antagonist
Prevent preterm labor
Nonapeptide analog of oxytocin that competitively inhibits the interaction of oxytocin with its membrane receptor on uterine cells result in in decreased frequency of uterine contractions

18
Q

Misoprostol and Alaprostadil

A

PGE1 analogs
Misoprostol administer orally or sublingually is used off label to stimulate uterine contractions and prevent treatment of postpartum hemorrhage
Alprostadil is a PGE1 analog used for its smooth muscle relaxing effects to maintain the ductus arteriosus patent in neonate so awaiting cardiac surgery
Suppository or injection of aloprostadil for erectile dysfunction

19
Q

Oxytocin

A

Uterine contractions
Labor inducing
Acts on receptors and increase Ca channels

20
Q

Ergonovine

A

Uterine contractions
Small doses can evoke rhythmic contractions of uterus and at high concentrations induce powerful and prolonged uterine contractions
At term uterus is more sensitive than earlier in pregnancy and far more sensitive than the non pregnant organ

21
Q

GI Motility

A

Mertoclopramide
Bethanechol
Erythromycin

22
Q

Metoclopramide

A

Dopamine D2 receptor antagonists
GI tract activation of dopamine receptors inhibits cholinergic smooth muscle stimulation
Blockade of this effect is primary effect of drug and increases esophageal peristaltic amplitude and increases lower esophageal sphincter pressure and enhances gastric emptying but have no effect on small intestine or colonoscopy motility
Anti nausea and Anti emetic action because of chemoreceptors trigger zone of medulla
Treat GERD, impaired gastric emptying and emesis
Toxicity: restlessness, drowsiness, insomnia, anxiety, agitation, short term use acute dystopia and long time tardive dyskinesia

23
Q

Bethanechol

A

Muscarinic receptor agonist
Not hydrolyzed by cholinesterase so long duration of action
Dry mouth and urinary retention from diabetic neuropathy

24
Q

Erythromycin

A

Macrolide antibiotics
Works on migrating motor complex to stimulate motilin receptors on GI smooth muscle and promote onset of MMC
Intravenous useful for gastroparesis
Tolerance develops rapidly
If upper GI hemorrhage then useful to promote gastric emptying

25
Q

Bronchodilators

A

B2 receptor agonists

Albuterol,,, Pirbuterol,, Terbutaline,,, Salmeterol,,, Formoterol

26
Q

Bronchodilators

A

Mechanism of action: B2 receptor agonist and cause bronchodilation via direct action on airway smooth muscles and inhibit release of bronchoconstricor mediators from inflammatory cells and inhibit NT from airway nerves
Relaxation of airway smooth muscle occurs via lowering of intracellular Ca, activation of K channels, and MLC phosphatase
Pulmonary airway action: bronchodilation, prevent micro vascular leakage and bronchial mucosa edema and increase mucous clearance
Long acting agonists–. Salmeterol, Formoterol (>12 hours and great for COPD)
Asthma and COPD–> terbutaline can be used to inhibit uterine contractions with premature labor
Toxicity–> tachycardia, muscle tremor, hypokalemia, V/Q mismatch (common with inhaled therapy)

27
Q

Anticholinergics

A

Ipratropium, Tiotropium

28
Q

Anticholinergics

A

Mechanism of action–> muscarinic receptor antagonist
Block contraction of airway smooth muscle and block increase secretion of mucus in response two vagal activity
Treat asthma and COPD
Toxicity- paradoxical bronchoconstriction (Ipratropium) and dry mouth (Tiotropium)

29
Q

Methylxanthine

A

Theophylline

Aminophylline

30
Q

Methylxanthine

A

Mechanism of action: theophylline is a bronchildator and effects in asthma and COPD
PDE inhibitor: non-selective to increase cAMP and cGMP to cause bronchodilation
Adenosine receptor antagonism–> bronchoconstriction and inflammation in airways of asthmatic patients by releasing histamine a and leukotriens
Other mechanism so: increase release of IL10 to prevent translocation of pro-inflammatory transcription factor NfKB to nucleus, promote apoptosis of T lymphocytes, eosinophils and activate histone deacetylase (HDAC 2) to enhance anti inflammatory effects of corticosteroids
Toxicity: nausea, vomiting , tremulousness, arrhythmias
narrow TI so monitor concentrations

31
Q

Pulmonary Hypertension

A

Epoprostenol, Iloprost (PGI2 analog)

Bosentan (Eta antagonist)

32
Q

Epoprostenol, Iloprost

A

MOA: prostacyclin (PGI2) lowers peripheral, pulmonary, coronary vascular resistance and
Epoprostenol is a PGI2 synthetic and has extremely short plasma half life of 3-5 min so continuous infusion
Iloprost is a PGI2 analog and half life of 30 min and inhaled six to 9 times per day
Treat pulmonary and secondary hypertension and treat portopulmonary hypertension in liver disease
Intravenous and inhalation
Toxicity–> flushing, headache, hypotension, nausea, diarrhea

33
Q

Pharmacological Actions of Vasodilator Drugs

A

NO
Increase or decrease cell membrane channel activity
Increase smooth muscle cell cAMP or cGMP levels
Activate vasodilator receptors
Inhibit vasoconstriction pathways and receptors

34
Q

Bosentan

A

Mechanism of action: ETa receptor antagonist
Endothelin-1 is a potent pulmonary vasoconstrictor that in produced in increased amount in PAH
ET1 contracts vascular smooth muscle and causes proliferation of ETa receptors
ETb release NO and PGI2 from endothelium to cause vaso relaxation
Bosentan is orally active combined ETa and ETb receptor antagonist that reduces symptoms and improves mortality of PAH
Intravenous and inhalation
Toxicity: liver toxicity, anemia, headaches, peripheral edema

35
Q

Ambrisentan

A

Orally active selective ETa receptor antagonist
Advantage to block only ETa receptors and allow ETb receptors to stimulate release of PGI2 and NO
Clinical efficacy of Bosentan

Pharmacology (12 decks)

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