ICD-10 Specific code I15: Secondary hypertension

Amlodipine is a calcium ion influx inhibitor of the dihydropyridine group (slow channel blocker or calcium ion antagonist) and inhibits the transmembrane influx of calcium ions into cardiac and vascular smooth muscle.

Benazepril is a prodrug which, after hydrolysis to the active substance benazeprilat, inhibits the angiotensin-converting enzyme (ACE) and so blocks the conversion of angiotensin I to angiotensin II. This reduces all the effects mediated by angiotensin II – i.e. vasoconstriction and production of aldosterone, which promotes the reabsorption of sodium and water in the renal tubules – and elevates cardiac output.

Candesartan is an AIIRA, selective for AT₁ receptors, with tight binding to and slow dissociation from the receptor. It has no agonist activity. The antagonism of the angiotensin II (AT₁) receptors results in dose related increases in plasma renin levels, angiotensin I and angiotensin II levels, and a decrease in plasma aldosterone concentration.

Chlortalidone is a benzothiadiazine (thiazide)-related diuretic with a long duration of action.

Cilazapril is a specific, long-acting angiotensin-converting enzyme (ACE) inhibitor which suppresses the renin-angiotensin-aldosterone system and thereby the conversion of the inactive angiotensin I to angiotensin II, which is a potent vasoconstrictor.

Dihydralazine is a member of phthalazines.

Diltiazem is a calcium antagonist. It restricts the slow channel entry of calcium into the cell and so reduces the liberation of calcium from stores in the sarcoplasmic reticulum. This results in a reduction of the amount of available intracellular calcium reducing myocardial oxygen consumption.

Enalapril is hydrolysed via hepatic CES 1 to the active metabolite enalaprilat, which acts as an ACE inhibitor. ACE is a peptidyl dipeptidase which catalyses the conversion of angiotensin I to the vasoconstrictor substance angiotensin II and hence inhibition of ACE results in decreased plasma angiotensin II. This also leads to increased plasma renin activity and decreased aldosterone secretion. The mechanism of action of enalapril is therefore primarily via the suppression of the RAAS. However, ACE is identical to kininase II, and so enalapril may also exert its effects by blocking the degradation of bradykinin, a potent vasodepressor peptide.

Isradipine is a potent dihydropyridine calcium channel blocker with selective activity on voltage-gated calcium channels (L-type or “long acting”). Isradipine has a higher affinity for such calcium channels in arterial smooth muscle than for those in the myocardium. It thus dilates arterial vascular beds, in particular those of the heart, brain and skeletal muscle without depressing cardiac function.

Lacidipine is a specific and potent calcium antagonist with a predominant selectivity for calcium channels in the vascular smooth muscle. Its main action is to dilate peripheral arterioles, reducing peripheral vascular resistance and lowering blood pressure.

Lisinopril is a peptidyl dipeptidase inhibitor. It inhibits the angiotensin-converting enzyme (ACE) that catalyses the conversion of angiotensin I to the vasoconstrictor peptide, angiotensin II. Angiotensin II also stimulates aldosterone secretion by the adrenal cortex. Inhibition of ACE results in decreased concentrations of angiotensin II which results in decreased vasopressor activity and reduced aldosterone secretion.

Nebivolol is a racemate of two enantiomers, SRRR-nebivolol (or d-nebivolol) and RSSS-nebivolol (or l-nebivolol). It is a competitive and selective beta-receptor antagonist and it has mild vasodilating properties due to an interaction with the L-arginine/nitric oxide pathway.

Nicardipine is a second generation slow calcium channel inhibitor, and belongs to the phenyl-dihydropyridine group. Nicardipine has a greater selectivity for L-type calcium channels in vascular smooth muscle than cardiac myocytes. Nicardipine produces smooth muscle relaxation and marked peripheral vasodilatation.

Olmesartan medoxomil is a potent, orally active, selective angiotensin II receptor (type AT₁) antagonist. It is expected to block all actions of angiotensin II mediated by the AT₁ receptor, regardless of the source or route of synthesis of angiotensin II. The selective antagonism of the angiotensin II (AT₁) receptors results in increases in plasma renin levels and angiotensin I and II concentrations, and some decrease in plasma aldosterone concentrations.

Piretanide is a loop diuretic for the management of fluid retention and treatment of mild to moderate hypertension.

Propranolol is a competitive antagonist at both beta, and beta₂-adrenoceptor, but has membrane stabilising activity at concentrations exceeding 1-3mg/litre, though such concentrations are rarely achieved during oral therapy. Competitive beta-blockade has been demonstrated in man by a parallel shift to the right in the dose-heart rate response curve to beta-agonists such as isoprenaline.