• Created by: MazzaW
  • Created on: 07-12-19 12:47

ACE inhibitors

Inhibits conversion of angiotensin I to angiotensin II, inhibits degradation of bradykinin (bradykinin produces vasodilation by release of vascular NO and prostaglandins), decreases aldosterone production, renal vasodilation

Indications: hypertension, HF, LV dysfunction, post-MI, diabetic nephropathy

Contraindications: pregnancy, hyperkalaemia, bilateral renal artery stenosis

Effectively combined with diuretics and CCBs

Side effects: dry cough, postural hypotension, teratogenic

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Inhibit action of endogenous angiotensin II at angiotensin II subtype 1 receptor (vasodilation and decreased sympathetic nervous system activity)

Does not block AT2 receptor which is exposed to high concentrations of angiotensin

Does not produce cough (unlike ACEi)

Indicated in hypertension when ACEis are contraindicated/not tolerated. Increasingly used in combination with ACEis in HF)

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Alpha blockers

Examples: prazosin, doxazosin

Block vascular smooth muscle alpha1 adrenoreceptors producing vasodilation leading to decreased blood pressure (baroreceptor-mediated increase in HR occurs)

First-dose phenomenon: large drop in BP occurs after 1st dose but not subsequent doses

Indications: prostatism, possible glucose intolerance

Contraindications: urinary incontinence, possible elderly + orthostatic hypotension

Effectively combined with beta-blockers

S/E: postural hypotension, headaches, nausea, ankle oedema, fatigue, sleep disturbance, occasionally erectile dysfunction

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Beta blockers

Decrease HR (decreased rate of spontaneous depolarisation, slow conduction in atria and AV node), decreased myocardial contractility, inhibition of RAA system, decreased peripheral resistance

Indications: angina, post-MI, tachycardias, possible HF, pregnancy and diabetes

Contraindications: asthma, COPD, heart block, possibly HF, PVD, hyperlipidaemia and physically active

Effectively combined with diuretics, CCBs (not verapamil), alpha blockers

S/E: bronchospasm, postural hypotension, bradycardia

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Calcium interacts with calmodulin to cause smooth muscle contraction. CCBs act on L-type voltage sensitive calcium channels to block calcium entry, causing vasodilation. They also inhibit the slow calcium current in the sinoatrial and AV nodes. High concentrations may inhibit the myocardial calcium entry causing a negative inotropic effect.

Haemodynamic effects: decreased peripheral resistance, decreased HR (diltiazem, verapamil), decreased coronary vascular resistance

May be rate-limiting (e.g. diltiazem, verapamil) or non-rate-limiting (e.g. nifedipine, amlodipine)

Indications: elderly with hypertension/IHD, Afro-Caribbeans with hypertension, angina (especially rate-limiting)

Contraindications: possibly right-sided HF

Effectivey combined with beta blockers (not verapamil), ACEis and alpha blockers

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Thiazide diuretics

Examples: bendroflumethiazide, chlortalidone, indapamide

Increased excretion of sodium/chloride/potassium/water, blocks Na-Cl cotransporter in distal nephron so more Na reaches distal tubule where some is exchanged by Na-K transport (increased potassium loss). BP lowering related to decreased peripheral resistance (unrelated to sodium loss)

Indications: HF, hypertension (3rd line)

Contraindications: gout, renal failure, possibly hyperlipidaemia, diabetes and sexually active males

Effectively combined with beta blockers and ACEis

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