Actions of angiotensin peptides on the rabbit pulmonary artery

Authors
Citation
Lmy. Tan et Mk. Sim, Actions of angiotensin peptides on the rabbit pulmonary artery, LIFE SCI, 66(19), 2000, pp. 1839-1847
Citations number
12
Categorie Soggetti
Biochemistry & Biophysics
Journal title
LIFE SCIENCES
ISSN journal
00243205 → ACNP
Volume
66
Issue
19
Year of publication
2000
Pages
1839 - 1847
Database
ISI
SICI code
0024-3205(20000331)66:19<1839:AOAPOT>2.0.ZU;2-R
Abstract
The presence of the angiotensin AT(1A)-like receptor subtype in the pulmona ry artery and AT(1B)-like receptor subtype in the pulmonary trunk of the ra bbit has been reported in two earlier studies. The present study further in vestigated these receptor subtypes using five other angiotensins (namely an giotensin II, angiotensin III, angiotensin IV, angiotensin-(1-7) and angiot ensin-(4-8)). The direct action of the angiotensins on the rabbit pulmonary arterial and trunk sections and the ability of each angiotensin to further contract or relax preconstricted sections of the pulmonary artery and trun k were studied using the organ bath set-up. The effects of angiotensin III on the H-3 overflow from re-uptaken [H-3]noradrenaline in the electrically- contracted rabbit pulmonary arterial and trunk sections were also studied. The contractile response of the arterial and trunk section had the followin g rank order potency: angiotensin II. angiotensin III. angiotensin IV. The contractile response to these angiotensins was greatly reduced or absent in the pulmonary trunk. Angiotensin II further contracted the preconstricted arterial and trunk sections. In contrast, angiotensin III further contracte d the preconstricted arterial section but relaxed the preconstricted trunk section. Angiotensin IV similarly relaxed the preconstricted trunk section but had minimum effect on the preconstricted arterial section. Angiotensin- (1-7) and angiotensin-(4-8) had no effect on both sections. The actions of the three angiotensins were inhibited by losartan, an AT(1)-selective antag onist. Indomethacin, a cyclo-oxygenase inhibitor, inhibited the relaxation caused by angiotensin III and angiotensin IV in the trunk section. The effe cts of angiotensin III on the electrically preconstricted sections of the p ulmonary trunk and artery were not accompanied by any significant changes i n H-3 overflow. The differential responses produced by angiotensin II and i ts immediate metabolites via two positionally located and functionally oppo sing receptor subtypes suggest that the pulmonary trunk and artery is not a passive conduit but an important regulator of blood flow from the heart to the lung.