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Potentiation of the hyporeactivity induced by in vivo endothelial injury in the rat carotid artery by chronic treatment with fish oil
Author(s) -
Joly Ghislaine A.,
Schini Valerie B.,
Hughes Helen,
Vanhoutte Paul M.
Publication year - 1995
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 - 10.1111/j.1476-5381.1995.tb15871.x
Subject(s) - in vivo , long term potentiation , medicine , fish <actinopterygii> , fish oil , carotid arteries , pharmacology , anesthesia , biology , fishery , microbiology and biotechnology , receptor
1 The present study investigates whether or not chronic feeding of rats with a diet enriched in fish oil affects the reactivity of balloon‐injured carotid arteries. The left carotid arteries were injured in vivo by the repeated passage of a balloon catheter. Both the right (control artery) and the left carotid arteries were excised 24 h after the injury, and suspended in organ chambers for the measurement of changes in isometric tension in the presence of indomethacin. 2 Phenylephrine evoked similar concentration‐contraction curves in the right (control) carotid arteries without endothelium from control and fish oil‐fed rats. Balloon injury decreased the contractility of carotid arteries to phenylephrine in both types of rats and the pEC 50 for phenylephrine was significantly decreased in balloon‐injured arteries from control rats compared to those obtained in arteries from fish oil‐fed rats (pEC 50 7.59 ± 0.1 and 7.28 ± 0.06, respectively) while maximal contractions were similar (1.93 ± 0.15 g and 1.79 ± 0.12 g, respectively). 3 The treatment of control right carotid arteries without endothelium with either N G ‐nitro‐ l ‐arginine (an inhibitor of nitric oxide synthase) or superoxide dismutase (which protects nitric oxide from degradation) did not affect significantly the contractions to phenylephrine in either group. In these preparations, methylene blue (an inhibitor of soluble guanylate cyclase) decreased slightly but significantly maximal contractions to phenylephrine in both groups. The treatment of balloon‐injured carotid arteries with N G ‐nitro‐ l ‐arginine or methylene blue partly restored contractions to phenylephrine in arteries from both types of rat. Superoxide dismutase further depressed the contractility to the α 1 ‐adrenoceptor agonist in balloon‐injured arteries from control diet‐fed rats but had no effect in balloon‐injured preparations from fish oil‐fed rats. 4 3‐Morpholino‐sydnonimine (SIN‐1, a donor of nitric oxide) evoked similar concentration‐dependent relaxations in control and balloon‐injured carotid arteries from both types of rat. 5 Balloon injury caused an increase in the tissue content of cyclic GMP in carotid arteries from control diet‐fed rats. This production of cyclic GMP was abolished by N G ‐nitro‐ l ‐arginine. Superoxide dismutase potentiated significantly the production of cyclic GMP caused by balloon injury in control but not in fish oil‐fed rats. 6 These observations confirm that in vivo balloon injury causes the production of nitric oxide in the injured blood vessel wall. This production of nitric oxide from l ‐arginine accounts for the decreased contractility to phenylephrine and the accumulation of cyclic GMP in balloon‐injured arteries. They further indicate that chronic feeding of rats with fish oil potentiates the l ‐arginine‐nitric oxide pathway in the injured vessel leading to an enhanced hyporeactivity to phenylephrine.