Angiotensin II relaxation of rainbow trout vessels in vitro

D. J. Conklin, Kenneth Olson

Research output: Contribution to journalArticle

35 Citations (Scopus)

Abstract

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 (1), 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 languageEnglish (US)
JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
Volume266
Issue number6 35-6
StatePublished - 1994
Externally publishedYes

Fingerprint

Trout
Oncorhynchus mykiss
Angiotensin II
Endothelium
Aorta
Vertebrates
Arteries
Saralasin
Rana catesbeiana
Losartan
Femoral Vein
Amphibians
Thoracic Aorta
Propranolol
Indomethacin
Prostaglandins
Arginine
Veins
Fishes
In Vitro Techniques

Keywords

  • amphibian
  • endothelium
  • endothelium-derived relaxing factor
  • fish
  • prostanoid
  • vasodilation

ASJC Scopus subject areas

  • Physiology

Cite this

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title = "Angiotensin II relaxation of rainbow trout vessels in vitro",
abstract = "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 (1), 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.",
keywords = "amphibian, endothelium, endothelium-derived relaxing factor, fish, prostanoid, vasodilation",
author = "Conklin, {D. J.} and Kenneth Olson",
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language = "English (US)",
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journal = "American Journal of Physiology",
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T1 - Angiotensin II relaxation of rainbow trout vessels in vitro

AU - Conklin, D. J.

AU - Olson, Kenneth

PY - 1994

Y1 - 1994

N2 - 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 (1), 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.

AB - 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 (1), 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.

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