Atrial natriuretic peptide contributes to the antihypertensive action of many drugs.

Data derived from a 10 years research program of our team demonstrate that many categories of antihypertensive drugs like beta-adrenergic blockers, alpha1-adrenergic blockers, ACE inhibitors, AT1-receptor antagonists and calcium-entry blockers increase plasma atrial natriuretic peptide (ANP) levels after a medium-term treatment of patients suffering from moderate essential hypertension. ANP always increases despite the drop of the arterial pressure and the fact that the left atrial and ventricular diameters remain unchanged or slightly reduced. These findings indicate that the increase of ANP plasma levels is not the result of a mechanical overload in the left cardiac chambers but the result of a pharmacological action. In conclusion, ANP is a universal factor contributing to the antihypertensive action of many drugs.

Beta-blockers and atrial natriuretic peptide (ANP) in hypertension.

Several studies (including ours) in patients with moderate hypertension indicate that beta-adrenergic blockers exert their antihypertensive action in part by increasing ANP secretion. There is also strong evidence that (beta 1- adrenergic receptors are mainly involved in this action. In this article we provide an overview on some of these studies.

ANP concentrations during interchanging DDD-VVI pacing modes in patients with retrograde ventriculoatrial conduction.

The main reason for the pacemaker syndrome during VVI pacing is the existence of ventriculoatrial conduction (V-AC). Twenty-five patients with a permanent DDD pacemaker and ventriculoatrial conduction were included in the study. IN those patients the hemodynamic changes were evaluated in relation to ANP plasma concentration changes during different modes of pacing. After a resting period of 30 minutes in the supine position ANP plasma concentration and blood pressure were evaluated: a) under DDD atrioventricular pacing at 90/min and for 30 minutes and b) under VVI pacing at 90/min and for 30 minutes. A decrease of systolic blood pressure by 12.77% (P < 0.0001) and diastolic blood pressure by 10.50% (P < 0.0001) was noticed during VVI pacing. ANP was increased during VVI pacing by 215.95% (P < 0.0001). It was observed that the acute transition from DDD to VVI pacing leads to a 3-fold increase in the levels of plasma ANP; this may be partially responsible for the pathogenesis of the haemodynamic changes during VVI pacing mediated through the direct hypotensive effect in addition to the coincidence of atrial and ventricular contraction. This study also proves the role of the increased systolic stress of atrial myocardium for the increased ANP secretion.