Effect of beta blockers on vascular resistance in systemic hypertension

Over 20 years ago, it was established that beta blockers could reduce high blood pressure. Currently, several beta blockers with different ancillary properties are available. They all have the property of blocking beta 1 receptors but differ from each other in a number of other respects: they may or may not block beta 2 receptors in low doses (beta 1 = receptor selectivity); they may or may not possess varying degrees of partial agonist activity, also known as intrinsic sympathomimetic activity (ISA); they vary in the extent to which they are soluble in fat (lipophilicity). A review of relevant published findings indicates that the effects of beta blockers on cardiac output are not essential for their antihypertensive effect, nor is penetration of these drugs into the brain and cerebrospinal fluid. Reduction in blood pressure during long-term beta blocker therapy is always associated with reduction of total peripheral resistance. Beta blockers with sufficient ISA to prevent cardio-depression, by exerting less negative inotropic and chronotropic effects on the heart, do not cause initial reflex vasoconstriction in response to cardiac beta blockade. Unlike beta blockers devoid of ISA, these agents ultimately reduce blood pressure by lowering the increased vascular resistance in hypertension to below pretreatment values. Recent beta blocker research has revealed a number of ways to manipulate the characteristically elevated vascular resistance in hypertension. Examples of these efforts are the combination of ISA, alpha 1 or alpha 2 receptor blockade and direct vasodilating properties in the enantiomers of a single beta blocker molecule. The practical significance of these developments remains to be established.