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Vasodilator effects of adrenomedullin on small pulmonary arteries and veins in anaesthetized cats
Author(s) -
Shirai Mikiyasu,
Shimouchi Akito,
Ikeda Soichiro,
Ninomiya Ishio,
Sunagawa Kenji,
Kangawa Kenji,
Matsuo Hisayuki
Publication year - 1997
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1038/sj.bjp.0701178
Subject(s) - adrenomedullin , vasodilation , medicine , pulmonary artery , calcitonin gene related peptide , lung , circulatory system , cats , anatomy , cardiology , endocrinology , receptor , neuropeptide
This study was conducted to determine adrenomedullin (AM) action sites in the pulmonary vascular bed and the relation between its vasodilator effects 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 μm i.d.) by use of an X‐ray televison system on the in vivo cat lung. 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 μm arteries (4±1, 11±2, and 17±2% with 0.01, 0.1, and 1 nmol kg −1 AM, respectively) was significantly larger than that for the veins (1±1, 5±2, and 7±2% with 0.01, 0.1 and 1 nmol kg −1 AM, respectively) whatever the injected dose of AM. When unilobar hypoxia (5% O 2 ) had decreased the i.d. of the 100–1100 μm arteries and veins by 16±3 and 6±3%, respectively, AM (0.1 nmol kg −1 ) was able to induce significantly larger i.d. increases in the arteries (28±3%) and veins (11±3%) than those under control conditions. The AM‐induced i.d. response pattern in the serially connected pulmonary arteries was quite different from that induced by CGRP; AM caused a greater increase in smaller vessels (100–500 μm) than in larger vessels (500–1100 μm). In the case of CGRP, a greater increase was observed in the larger vessels. CGRP 8–37 (100 nmol kg −1 , i.v., followed by a continuous infusion of 0.2 nmol kg −1 min −1 ) had no significant effect on the i.d. increase induced by AM (0.1 nmol kg −1 ) in any serial segments of the arteries and veins. 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 μm). The vasodilator effect 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 specific receptor.British Journal of Pharmacology (1997) 121 , 679–686; doi: 10.1038/sj.bjp.0701178