Cardiovascular Pharmocology - Drug Names And Moa

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Beta- Blockers

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'olol drugs
3 generations
MOA: Inhibit binding of Noradrenalin and Adrenalin to β-receptors.
EFFECTS: ↓ CO and BP, -ve chronotrope, -ve inotrope (↓O2 consumption), ↓ Renin
Long term = ↓TPR

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Metaprolol

Back 2

CLASS: 2nd generation β-Blocker

β1 selective, so don’t have as much affect on the airways. Can still be some cross-reaction.

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Atenolol

Back 3

CLASS: 2nd generation β-Blocker

β1 selective, so don’t have as much affect on the airways. Can still be some cross-reaction.

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Propanolol

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CLASS: 1st generation β-Blocker

Non-selective - can be airways issues.

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Clonidine

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CLASS: α2 agonist
MOA: Agonist on α2 receptor (preganglionic sympathetic terminal) causes blocking NA release so the post-ganglionic cell is not acted on.
EFFECT: Reduce BP by ↓ symp. effect on CO and peripheral vasculature.

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α-Methyldopa

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CLASS: α2 agonist
MOA: Broken down to form α-methy NA ( an alpha 2 agonist) in synaptic terminals

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Doxazosin

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Selective α1 blocker on vasculature
Blocks vasoconstriction – acts as vasodilator
Less reflex tachycardia than non-selective α-blockers
↓Arteriolar resistance

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Cilazipril

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CLASS: ACE Inhibitor
MOA: Inhibit ACE (angiotensin converting enzyme)
EFFECTS: ↓ levels of ATII – reduces systemic vascular resistance (afterload) and Vasodilation of veins (↓ pre-load)
↑bradykinin levels, ↓ ATII provoked sympathetic activity - promote vasodilation
Block ATII effect in kidney
↓Aldosterone
↑Na and water excretion, ↓Plasma volume, ↓BP

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Losartan

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CLASS: Angiotensin Receptor Blocker (ARB)
MOA ATII receptor antagonists/blockers
Potent selective AT1 receptor antagonists – block all ATII effects on AT1 receptors
EFFECT: Prevent vascular smooth muscle contraction and Aldosterone secretion

Effect limited to AT1 – AT2 beneficial no kinin acc. ↓cough

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Acetylsalicylate

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CLASS: Asprin - Anti-platelet
MOA: Non-selective COX inhibitor
Irreversibly acetylates platelet COX-1 reducing TXA2 prod for the lifetime of the platelet (7-9 days)
Acts on platelets in portal circulation before being metabolised in liver

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Clopidogrel

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CLASS: Antiplatelet
MOA: Non-competitive inhibitor of ADP (P2Y) receptors
Prevent activation of GPIIb/IIIa receptor
Reduces platelet activation
Synergistic with aspirin

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Unfractionated (UF) Heparin

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CLASS: Anti-coagulant
MOA: Reduces the formation of fibrin by ↑ action of ATIII binding with FXa and Thrombin (FIIa)

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Enoxaparin

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CLASS: Low molecular weight Heparin (LMWH) - Anticoagulant
MOA: Potentiates (increases power of) the action of ATIII on FXa and has less effect on thrombin.

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Warfarin

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CLASS: Coumarin - Anticoagulant
Prevents the reduction of Vit K by inhibiting vit K epoxide reductase – leaving it inactive
And stopping it from activating FII, FVII, FXI, FX and protein C & S
EFFECT: Overall reduced formation of fibrin

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Dabigatran

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CLASS: Anti-coagulant
MOA: A competitive and reversible direct thrombin inhibitor

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Alteplase

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CLASS: Fibrinolytic
MOA: Recombinant Tissue Plasminogen Activator (rt-PA - Serine protease
Converts plasimogen to plasmin
EFFECT: Helps break down a previously formed thrombus
Normally synthesised by endothelial cells

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Felodipine

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CLASS: Calcium Channel Blocker
Dihydropyridine (Vasoselective)
MOA: Inhibit Ca2+ influx through L-type and T-type calcium channels (LTCCs) by binding to and stabilising the CLOSED channel state – more likely in smooth muscle b/c depolarisations last longer than in cardiac muscle
EFFECTS: Act on Ca2+ entry into:
Vascular (arteriolar) smooth muscle – vasodilate
↓vascular resistance (afterload)
Little effect on venous beds – no effect on preload

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Verapamil

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CLASS: Calcium Channel Blocker
Phenylalkylamine (Cardioselective)
MOA: Inhibit Ca2+ influx through L-type calcium channels (LTCCs) binding during their OPEN state
Suppresses cardiac contractility and O2 consumption
Channel inhibition increases at higher heart rates
EFFECTS: Cardiac muscle (-ve inotrope)(↓contraction)
SA nodal tissues (-ve chronotrope)↓contraction
AV node: ↓conduction (-ve dromotrope)
Decreases HR node conduction velocity

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Dilitiazem

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CLASS: Calcium Channel Blocker
Benzothiazipine (Cardioselective)
MOA: Inhibit Ca2+ influx during membrane depolarisation of primary cardiac and vascular smooth muscle
Interferes with slow inward (depol) current in excitable cardiac tissue – suitable as anti-arrhythmic

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Glyceryl trinitrate (GTN)

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CLASS: Nitrodilator - Antianginal
MOA: Vasodilate venous circulation = ↓preload and O2 demand
Reduce systemic arterial resistance = ↓afterload

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Isobide dinitrate

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CLASS: Nitrodilator - Antianginal
MOA: Vasodilate venous circulation = ↓preload and O2 demand
Reduce systemic arterial resistance = ↓afterload

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Sodium Nitroprusside

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(ferricyanide)
Produce controlled rapid hypotension in surgery – but very dangerous and can’t give much

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Mannitol

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CLASS: Osmotic Diuretic
SITE: Proximal Tubule/Loop
MOA: Filtered in glomerulus but poorly reabsorbed – keeps water in tubule with it – osmotically active drug

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Frusemide

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CLASS: Loop Diuretic
SITE: Thick ascending limb (TAL)
MOA: Inhibits luminal NKCCK (Na+2Cl-K+) Cotransporter (competes with Cl-)
EFFECT: Prevents reabasorption of all 3.
Also removes negative pd across cell – no gradient to pull Na+, Ca2+,Mg2+ to basolateral side so ↑ excretion.
Also increases H+ and K+ loss at distal tubule

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Bendroflumethiazide

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CLASS: Thiazide Diuretic
SITE: Distal tubule
Secreted in proximal tubule
MOA: Competitively bind to eNCC1 Na+Cl- cotransporter.
Inhibit Na+/Cl- cotransport and reabsorption in cortical diluting segment of distal tubule (5% Na)
EFFECTS: Modest increase in Na and water secretion – leads to K+ loss also
eNCC1 is upregulated by aldosterone.

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Spironolactone

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CLASS: K+ Sparing Diuretics
Mineralcorticoid receptor inhibitors
SITE: Late distal, collecting duct
Aldosterone antagonist – competitively binds and prevents translocation of mineralcorticoid receptor.
On basolateral (blood) side so doesn’t require access to lumen.
EFFECTS: Blocks aldosterone pathway – decreases expression of ENaC and Na+/K+ ATP pump - ↑Na+ loss (no reabs.)

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Lignocaine

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CLASS: Na+ Channel Blocker - Local Anaesthetic, Antiarrhythmic

MOA: Block fast Na+ channels in a use-dependent way – binds most strongly to open and inactivated (plateau) channels.
No AP = no conduction.

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Amiodarone

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CLASS: K+ Channel Blocker - Antiarrythmic
MOA: Block K+ channels involved in membrane repolarisation
Modulate lipid membrane properties and affect Na+ fluxes and Ca2+ channels (affects both SA & AV nodes)
EFFECT: Plateau and AP duration are prolonged

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Digoxin

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CLASS: Cardiac glycoside - Heart Rate Control/Heart Failure
MOA: Increases force of contraction and slows rate 2 mechanisms
1) Inhibit cellular Na+/K-ATPase - ↑intracellular Na+ -> ↑intracellular Ca2+
-> ↑ force of contraction
↑CO, ↓symp tone, ↑urine, ↓Renin
2) ↑ vagal activity to the heart (Ach)
↓ SA firing rate ↓HR
Reduces conduction velocity through AV node ↓HR

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Atorvastatin

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CLASS: Statin - Lipid-lowering
MOA: Reversible, competitive HMGCoA inhibitors
Decrease mainly hepatic de novo synthesis of cholesterol
Also increase activity of eNOS (NO prod) - vasodilation
↑LDL-r synthesis - ↑ clearance of LDL and ↓ plasma LDL cholesterol and TAGs
Slight ↑ in plasma HDL
Statins also inhibit transcription factor pathways – reduce inflammatory processes

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Bezafibrate

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CLASS: Fibrate - Lipid-lowering
MOA: PPARα (peroxisome proliferator activated receptor) activators
↓ApoCIII synthesis (an inhibitor of lipoprotein lipase)
↑FA oxidation in muscle and liver and lipogenesis in the liver
↓LDL by shifting hepatocyte metabolism toward FA oxidation
↑Apo AII synthesis - ↑HDL