The effects of salmonid angiotensin II ([Asn1,Val5]ANG II) were examined in isolated trout arteries [celiacomesenteric (CMA), coronary (COA), 3rd or 4th gill arch epibranchial (EBA), ventral aorta (VA)] and veins [anterior cardinal (ACV) and ductus Cuvier strips (DOC)]. ANG II (10-10-10-6 M) produced modest (<50% other agonists) transient contractions in otherwise unstimulated COA but was a poor agonist in other vessels. In precontracted vessels, ANG II responses were triphasic; transient contraction (P1), relaxation (P2), and partial recovery (P3) and vessel specific. P1 was similar to uncontracted vessels. With 10-6 M ANG II, %P2 was: EBA, 60.3 ± 8.3% (n = 22); CMA, 48.8 ± 8.8% (n = 4); ACV, 38.8 ± 5.3% (n = 29); VA, 29.4 ± 4.9% (n = 8); DOC, 25.5 ± 2.4% (n = 14); COA, 13.2 ± 6.7% (n = 4). P2 in EBA and ACV was dose dependent [EBA vs. ACV: mean effective concentration (EC50) = 3.6 x 10-9 ± 8.1 x 10-10 M, n = 7 vs. 6.2 x 10-8 ± 2.3 x 10-8 M, n = 8, respectively; P ≤ 0.05] and inhibited by indomethacin but unaffected by propranolol, N(G)-monomethyl-L-arginine, saralasin, PD-123177, or DuP-753. Removal of EBA endothelium also inhibited relaxation. By comparison, ANG II did not relax bullfrog arteries (dorsal aorta, systemic arch, CMA) or femoral veins. These results show that, in large vessels of trout, the predominant effect of ANG II is an endothelium- dependent, prostanoid-mediated relaxation that is unaffected by classical ANG II-receptor antagonists. ANG II-mediated relaxations, therefore, appeared early in vertebrate evolution; they may have been deleted from amphibia, or evolved independently in fish and endothermic vertebrates.
|Original language||English (US)|
|Journal||American Journal of Physiology - Regulatory Integrative and Comparative Physiology|
|Issue number||6 35-6|
|State||Published - Jan 1 1994|
- endothelium-derived relaxing factor
ASJC Scopus subject areas
- Physiology (medical)