ISSN:
1432-1912
Keywords:
Canine thoracic aorta
;
PGI2 and 6-keto PGF1α
;
Endothelium dependent relaxation
;
PGI2-induced vasodilation
;
Acetylcholine-induced vasodilation
Source:
Springer Online Journal Archives 1860-2000
Topics:
Medicine
Notes:
Summary In circular-cut strips prepared from canine thoracic aorta, acetylcholine (ACh) and A23187 relaxed endothelium-intact tissues [E(+) preparations] pre-contracted with noradrenaline or excess concentrations of K. These relaxations were associated with marked increases in the amount of 6-keto PGF1α. After removal of the endothelium [E(−) preparations] the relaxation ceased, and the amounts of 6-keto PGF1α were markedly reduced. In E(+) preparations, application of indomethacin attenuated the increase in 6-keto PGF1α induced by ACh or A23187 in the presence of noradrenaline or high K, but not the endothelium-dependent relaxations. In E(−) preparations, ACh (0.1–10 μM) neither increased the amount of 6-keto PGF1α nor produced a contraction. In dispersed single endothelial cells, A23187 markedly increased but 118 mM K did not modify the amount of 6-keto PGF1α. Both noradrenaline and high K increased the production of 6-keto PGF1α in the E(−) preparations but to a lesser extent than that in the E(+) preparations. This action was attenuated by indomethacin. The amplitude of the noradrenaline-and K-induced contractions was enhanced with indomethacin pretreatment in both E(+) and E(−) tissues. PGI2-Na (10 nM), reduced the amplitude of noradrenaline-induced contractions, concentration dependently and to the same extent in both E(+) and E(−) preparations. These results indicate that synthesis of PGI2 in the endothelium is not causally related to the endothelium dependent relaxation. PGI2 synthesized in the endothelium may not act directly on the muscle tissue, but PGI2 synthesized in the smooth muscle tissue may produce an inhibition of contraction.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/BF00512944
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