ABSTRACT
Elevated blood pressure (BP) accelerates microvascular and macrovascular disease. Antihypertensive agents are widely prescribed. They include:
β-blockers (e.g. atenolol):
– the precise antihypertensive action of β-blockers is poorly understood
– reduce cardiac output, alter baroreflex sensitivity and block peripheral adrenoreceptors
– it is possible that their antihypertensive effect is central
α-blockers (e.g. prazosin):
– reduce BP by blocking post-synaptic α-receptors, causing vasodilatation
calcium channel blockers (e.g. nifedipine):
– act by blocking calcium influx through the slow transmembrane calcium channels
– dihydropyridine calcium channel blockers such as nifedipine cause vasodilatation alone; non-dihydropyridine calcium channel blockers such as verapamil are also negative ionotropes
angiotensin-converting enzyme (ACE) inhibitors (e.g. ramipril):
– block the conversion of angiotensin I to angiotensin II
– reduction in angiotensin II levels leads to reduced salt and water retention and vasodilatation
– particularly useful in diabetic patients in whom they may protect against nephropathy
angiotensin II antagonists (e.g. losartan):
– used in those intolerant of ACE inhibitors, these drugs directly inhibit angiotensin II
– actions are identical to ACE inhibitors
nitrates (e.g. glyceryl trinitrate):
– reduce blood pressure through a direct vasodilatating action on smooth muscle
central-acting antihypertensives (e.g. methyldopa):
– mode of action is uncertain.
