Acute volume loading, atrial natriuretic peptide release and cardiac function in healthy men. Effects of beta-blockade

Release of ANP is dependent on right atrial distension and pressure, which in turn are dependent on both venous return and left ventricular function. These two latter parameters are both modulated by beta-receptors. In the present study, the effects of selective beta-blockade vs non-selective beta-blockade on hypertonic volume expansion induced changes in ANP release and systemic hemodynamics were assessed in 8 healthy normotensive male volunteers. On placebo, infusion of hypertonic saline (1200 ml of 2.5% NaCl) caused an intravascular volume expansion of 10-11%, and small non-significant increases in cardiac performance (LVEDV, SV, or CI), but it provoked a 2-fold increase in plasma ANP. Beta-blockade by either atenolol or propranolol blunted the increase in cardiac volume load (reflected by LVEDV) as compared to placebo, but did not affect the ANP response to volume expansion. The increase in ANP correlated closely with the intravascular volume expansion on placebo and to a lesser extent on beta-blockade. In healthy men, therefore, intravascular volume expansion that caused only small changes in cardiac activity, resulted in clear increases in release of ANP. Inhibition of the increase in cardiac volume load by beta-blockade did not interfere with ANP increase, suggesting a role for extra-cardiac receptors in the release of ANP or a change in the pressure/volume relationship.