Sustained essential hypertension is characterised by a progressive decline in renal blood flow and a progressive increase in renal vascular resistance, while glomerular filtration rate remains normal or is reduced to a lesser extent. Renal blood flow is not only decreased per unit square metre of body surface area but also as a fraction of cardiac output. Although the precise mechanism of this renal haemodynamic abnormality remains speculative, the possibility that the renal vasculature plays a role in the pathogenesis of essential hypertension is receiving major attention. Different antihypertensive drugs have different renal haemodynamic effects. Nonselective beta-blockers generally tend to cause a modest decrease in renal blood flow but certain beta-blockers (including those with cardio-selectivity or intrinsic sympathomimetic activity) appear to cause less of a reduction in renal haemodynamics than others. Adrenergic blocking agents and diuretics do not produce clinically relevant renal haemodynamic changes, and data obtained with vasodilators are conflicting. Most studies with calcium antagonists show a renal vasodilator response. Angiotensin-converting enzyme inhibitors increase renal blood flow and decrease renovascular resistance in essential hypertension.