The sympathetic nervous system plays a major role in the pathogenesis of essential hypertension and is mediated by the α and β receptors. The α receptor is divided into two types, α₁ and α₂ based on response to epinephrine and norepinephrine. α₁‐Adrenergic receptors have a high affinity for drugs such as prazosin, doxazosin, and terazosin, which act to reduce blood pressure by selective blockade of the receptor. These agents provide a rational approach to the treatment of hypertension by correcting elevated total peripheral resistance, the fundamental hemodynamic abnormality in essential hypertension. In contrast, early α‐adrenergic receptor blockers nonselectively blocked both α₁ and α₂ receptors and were unsuitable as antihypertensive agents because they induced tachycardia and patients developed a tolerance to them rapidly. α₁‐Adrenergic blockers also have beneficial effects on plasma lipoproteins, tending to decrease levels of triglycerides and cholesterol and increase levels of high‐density lipoprotein (HDL) cholesterol and the HDL cholesterol/total cholesterol ratio. β‐Adrenergic blockers, such as propranolol and atenolol, have been shown to have an adverse effect on the lipid profile by tending to increase levels of triglycerides and decrease HDL cholesterol. A number of mechanisms contribute to these effects, in particular, adrenergic modulation of lipoprotein lipase and the triglyceride secretion rate. Doxazosin has been shown to increase the activity of LDL receptors, which may be partly responsible for its beneficial effect on plasma lipids and lipoproteins. Doxazosin is different from other α₁ adrenergic inhibitors in that its maximal hypotensive effect occurs within 5 or 6 hours after administration in acute dosing studies, making first‐dose postural hypotension unlikely, and its long half‐life provides 24‐h blood pressure control with once‐daily dosing.