We examined whether adrenomedullin, a vasoactive peptide expressed in the heart, modulates the increase in blood pressure, changes in systolic and diastolic function and left ventricular hypertrophy produced by long-term administration of angiotensin II or norepinephrine in rats. Subcutaneous administration of adrenomedullin (1.5 µg/kg/h) for one week inhibited the angiotensin II-induced (33.3 µg/kg/h s.c.) increase in mean arterial pressure by 67 % (P<0.001), but had no effect of norepinephrine-induced (300 µg/kg/h s.c.) hypertension. Adrenomedullin enhanced the angiotensin II-induced improvement in systolic function, resulting in a further 9 % increase (P<0.01) in the left ventricular ejection fraction and 19 % increase (P<0.05) in the left ventricular fractional shortening measured by echocardiography, meanwhile norepinephrine-induced changes in systolic function were remained unaffected. Adrenomedullin had no effect on angiotensin II- or norepinephrine-induced left ventricular hypertrophy or expression of hypertrophy-associated genes, including contractile protein and natriuretic peptide genes. The present study shows that adrenomedullin selectively suppressed the increase in blood pressure and augmented the improvement of systolic function induced by angiotensin II. Since adrenomedullin had no effects on angiotensin II- and norepinephrine-induced left ventricular hypertrophy, circulating adrenomedullin appears to act mainly as a regulator of vascular tone and cardiac function.