Possible significance of the pharmacological differentiation of beta‐ blockers for therapy of hypertension.

Abstract

1 Cardioselective and non-selective P-blockers affect to a different degree several aspects of the circulatory homeostasis. The evidence available in this regard has been evaluated and the possible clinical importance of these differences has been discussed.2 Venous return is partly regulated by P-receptors (possibly of the f2 type) in the venous resistance vessels. Differences in blockade of venous return by the two classes of P-blockers may, therefore, influence the degree of increase in left ventricular size, left ventricular end diastolic BPs and stroke volume during P-blockade.3 At the first part of the dose-response curve, non-selective f-blockers seem to block more effectively renin release than cardioselective P-blockers. 4 The direction and the extent to which P-blockers 'directly' affect total peripheral resistance (TPR), is determined by the resultant of the degree of decrease in TPR by blockade of renin release and the extent of the increase in TPR by blockade of the P2-receptors in the arteriolar wall.5 The clinical relevance of these differences could be that especially in the low doses range non-selective P-blockers may be more 'safe' in patients with compromised cardiac function and may be more appropriate for the therapy of high renin hypertension than cardioselective blockers, whereas the latter may be more appropriate for the majority of hypertensive patients who have lowto normal renin hypertension.

Clinical utility of fixed-dose combinations in hypertension: evidence for the potential of nebivolol/valsartan

“…Thus, the BP-lowering effect of traditional β-blockers with no vasodilatory ability (ie, atenolol, metoprolol, propranolol) is achieved through a decrease in central nervous system sympathetic outflow, 31 reduced cardiac output consequent to decreased heart rate and contractility, and reduced renin release. 41 The magnitude of the antihypertensive response may be offset by compensatory vasoconstriction in the peripheral vasculature 31 , 42 and negative effects on metabolic parameters and lipid profile, 43 as well as increased venous return mediated by β 2 -adrenergic receptor blockade enlarging the left ventricle. 42 …”

“… 41 The magnitude of the antihypertensive response may be offset by compensatory vasoconstriction in the peripheral vasculature 31 , 42 and negative effects on metabolic parameters and lipid profile, 43 as well as increased venous return mediated by β 2 -adrenergic receptor blockade enlarging the left ventricle. 42 …”