Background: Experimental study has shown that blunted arterial baroreflex function markedly attenuated inotropic responses to a phosphodiesterase inhibitor (PDEI) even in normal hearts. However, whether arterial baroreflex function is related to the inotropic responsiveness to a PDEI has not been clarified in human heart failure (HF). Hypothesis: The goal of this study was to examine the relationship between inotropic responses to a PDEI and arterial baroreflex sensitivity in human HE Methods: Twelve patients with HF were examined, and hemodynamic responses to milirinone (12.5,25, and 50 mu g/kg, intravenous injection) and arterial baroreflex sensitivity were assessed by pulse interval-left ventricular (LV) systolic pressure slope using nitroglycerin and phenylephrine. Results: Milrinone (25 mu g/kg) significantly increased LV dP/dt. Arterial baroreflex sensitivity was only one predictor of inotropic responses to milrinone by multivariate analysis; a strong positive correlation was also found between LV dP/dt and baroreflex sensitivity (y = 6.656x -3.326, r = 0.93, p = 0.000). Conclusion: Inotropic effects of milrinone, a PDEI, correlated significantly with arterial baroreflex sensitivity, suggesting that the more baroreflex function was impaired, the more the inotropic effect of a PDEI was depressed in human HF.