This chapter is probably relevant to Section G8(iii)  of the 2017 CICM Primary Syllabus, which asks the exam candidate to "understand the pharmacology of anti-hypertensive drugs". Rather than diving deep into the minor details of each class, it serves as a jumping point to all antihypertensive questions in the CICM primary. They are numerous, as you can see. For the majority of these, little analytical though it called for - they ask for rote-learned pharmacokinetic data and memorised details. Fortunately for the candidates, it appears that many of these are repeated, and there is only a limited range of drugs which keeps appearing:

  • Question 14 from the second paper of 2019 (compare metoprolol and esmolol)
  • Question 8 from the second paper of 2017 (calcium channel blockers, nimodipine)
  • Question 11 from the first paper of 2015 (sodium nitroprusside toxicity)
  • Question 2 from the first paper of 2014  (calcium channel blockers, verapamil)
  • Question 10 from the first paper of 2013 (carvedilol and spironolactone, weirdly)
  • Question 17 from the second paper of 2011 (calcium channel blockers)
  • Question 24 from the second paper of 2010 (antihypertensives in general)
  • Question 4(p.2) from the first paper of 2010 (metoprolol and GTN)
  • Question 9(p.2) from the second paper of 2008 (ACE-inhibitors and ARBs)
  • Question 8(p.2) from the second paper of 2008  (sodium nitroprusside and GTN)
  • Question 3(p.2) from the first paper fo 2008 (sodium nitroprusside and GTN)

However, on occasion they might ask you to classify antihypertensive agents, as in Question 24 from the second paper of 2010. 

To answer, you could potentially produce a nesting hierarchical structure, if that is the sort of thing that appeals to you. It would be something like:

  • Sympatholytic drugs
    • Beta-blockers
      • Selective beta-1 blockers
      • Non-selective beta-blockers
    • Alpha-1 blockers
    • Alpha-2 agonists

However, this unordered list does not meet the requirements of the college examiners, who also needed "a brief outline of each mechanism, and an example of a drug in each class". That sort of thing really lends itself to a tabulated format.  So,  here is a loosely unstructured table similar to the one used to answer that SAQ.

Classification of Antihypertensive Agents
Class Mechanism Examples

RAAS antagonists

Renin antagonists Inhibits the activity of renin, which reduces the activation of angiotensin , thus prevents RAAS activation Aliskiren


Interrupts the conversion of Ang-I into Ang-II, thereby interrupting the effects of RAAS activation Perindopril

Angitensin receptor blockers

Interferes with the binding of Ang-II and its AT1 receptor. Irbesartan

Sympatholytic drugs

Beta blockers

Selective (β1)

By binding to Gs-protein coupled β1 and β2 receptors, blocks cAMP synthesis

Non-selective Propanolol
Alpha-1 blockers Reversible By inding to the Gq-protein-coupled alpha-1 receptor, this drug decreases the activation of phospholipase C, resulting in a decreased concentration of the secondary messengers IP3 and DAG. The result is decreased intracellular calcium availability, which in turn leads to decreased smooth muscle contraction tone. Prazocin
Irreversible Phenoxybenzamine
Alpha-2 agonists Central alpha-2 agonist effect decreases sympathetic outflow by presynaptic downregulation of noradrenaline release. Clonidine
Ganglionic blockers Blocks ganglionic autonomic neurotransmission by inhibiting the nicotinic Ach receptors, therefore decreasing both sympathetic tone and vagal neurotransmission. Hexamethonium
Monoamine transport inhibitors Blocks VMAT-2 in the adrenergic neurotransmission pathway, causing the depletion of catecholamine and serotonin stores in central and peripheral nerve terminals Reserpine
Catecholamine synthesis inhibitors By inhibiting the conversion of tyrosine into dopa, blocks the synthesis of catecholamines α-methyltyrosine


Calcium channel blockers Dihydropyridine Modulates the opening of voltage-gated calcium channels, which prevents  intracellular calcium influx during depolarisation. This decreases the availability of intracellular calcium for vascular smooth muscle cells, decreasing their resting tone. In cardiac myocytes, this decreases contractility as well as the automaticity of pacemaker cells. Amlodipine
Non-dihidropyridine Verapamil
Nitrate vasodilators
(nitric oxide donors)
Acts as donor of nitric oxide (NO) which activates guanylate cyclase, resulting in an increase of cyclic GMP in vascular smooth muscle. This hyperpolarises the membrane by increasing potassium channel conductivity and decreases the availability of inracellular calcium, thereby decreasing the resting tone and contractility of vascular smooth muscle GTN
Potassium channel activators Activates ATP-sensitive potassium channels which inhibits the opening of voltage-dependent calcium channels indirectly, by hyperpolarising the membrane. Hydralazine
Phosphodiesterase inhibitors Increases cyclic AMP by inhibiting phosphodiesterase (with maximum selectivity for PDE10), which is responsible for cAMP catabolism. Selective for vascular smooth muscle. Papaverine

Some duplication of drugs here was necessary, and mildly annoying. Consider: methyldopa also acts a a catecholamine synthesis inhbitor, nicorandil has nitrate vasodilator effects, labetalol has beta and alpha blocking properties, so these classes clearly overlap to a considerable degree. Moreover, the textbooks typically all produce classification systems which are a) unlike the one offered here, and b) totally different to one another.  In short, one should not take this proposed classification system as something  credible or highly scientific, as it was created by a crazy person during a bout of insomnia.