1 This study was conducted to determine adrenomedullin (AM) action sites in the pulmonary vascular bed and the relation between its vasodilator e ects and vascular tone. Moreover, an examination was made into whether calcitonin gene-related peptide (CGRP) receptors mediate pulmonary vasodilatations induced by AM. To this end, we directly measured internal diameter (i.d.) changes in small pulmonary arteries and veins (100 ± 1100 mm i.d.) by use of an X-ray televison system on the in vivo cat lung. 2 Under control (resting vascular tone) conditions, AM injections into the left main pulmonary artery caused dose-related i.d. increases in both small arteries and veins. The mean i.d. increase of the 100 ± 1100 mm arteries (4+1, 11+2, and 17+2% with 0.01, 0.1, and 1 nmol kg 71 AM, respectively) was signi®cantly larger than that for the veins (1+1, 5+2, and 7+2% with 0.01, 0.1 and 1 nmol kg 71 AM, respectively) whatever the injected dose of AM. 3 When unilobar hypoxia (5% O 2 ) had decreased the i.d. of the 100 ± 1100 mm arteries and veins by 16+3 and 6+3%, respectively, AM (0.1 nmol kg 71 ) was able to induce signi®cantly larger i.d. increases in the arteries (28+3%) and veins (11+3%) than those under control conditions. 4 The AM-induced i.d. response pattern in the serially connected pulmonary arteries was quite di erent from that induced by CGRP; AM caused a greater increase in smaller vessels (100 ± 500 mm) than in larger vessels (500 ± 1100 mm). In the case of CGRP, a greater increase was observed in the larger vessels. 5 CGRP 8 ± 37 (100 nmol kg 71 , i.v., followed by a continuous infusion of 0.2 nmol kg 71 min 71 ) had no signi®cant e ect on the i.d. increase induced by AM (0.1 nmol kg 71 ) in any serial segments of the arteries and veins. 6 The results indicate that, in the cat, AM induces greater vasodilatation in small pulmonary arteries and lesser vasodilatation in small veins, the maximum dilatation being in the more peripheral arterial segment (100 ± 500 mm). The vasodilator e ect of AM was enhanced when vascular tone was elevated. The data suggest that the AM-induced pulmonary vasodilatation is not mediated by CGRP receptors but by its own speci®c receptor.