THE DESIGNATION of α- and β-adrenergic receptors in vascular smooth muscle 1 has proved useful in describing adrenergic function. Alpha-receptors, when stimulated, produce peripheral vasoconstriction which can be blocked by such pharmacological agents as phenoxybenzamine or phentolamine. Stimulation of β-receptors produces increased inotropic and chronotropic myocardial activity, as well as peripheral vasodilation; these responses can be blocked by dichloroisoproterenol, pronethalol, or propranolol.
Use of β-adrenergic blocking drugs in treatment of hypertension may at first seem paradoxical, since inhibition of a neural mechanism serving vasodilation is contrary to current physiological thinking. However, vascular resistance is not the sole determinant of pressure; blood flow is the other dependent variable. If, therefore, elevated blood pressure could be ascribed to an increase in flow or its determining variables, heart rate and stroke volume, normalization of these factors may provide a specific therapeutic measure in its reduction. Increased β-activity can, therefore, produce hypertension if blood