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Interactions of palmitoyl carnitine with the endothelium in rat aorta
Author(s) -
Dainty I.A.,
Bigaud M.,
McGrath J.C.,
Spedding M.
Publication year - 1990
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.1476-5381.1990.tb15789.x
Subject(s) - endothelium derived relaxing factor , sodium nitroprusside , endocrinology , acetylcholine , medicine , chemistry , endothelium , aorta , stimulation , biology , nitric oxide
1 Palmitoyl carnitine (10–1000 μ m ) resembled Bay K 8644 (10–1000 n m ) in that it directly contracted rat aortic rings which were partially depolarized with K + (12 m m ). However, the effects of Bay K 8644 were reduced in the presence of endothelium whereas the presence of the endothelium hardly affected the palmitoyl carnitine‐induced contractions, which occurred at high concentrations (< 10 μ m ). 2 Lower concentrations of palmitoyl carnitine (0.3–30 μ m ; EC 50 1.1 μ m ), but not Bay K 8644, carnitine or palmitic acid, antagonized the relaxant effects of acetylcholine in rat aorta. The antagonism was specific for endothelium‐dependent relaxations, in that the relaxations to ATP and the calcium ionophore A23187 were also non‐competitively antagonized, albeit at slightly higher concentrations, whereas the direct relaxant effects of sodium nitroprusside were unaffected. Palmitoyl carnitine therefore antagonizes the effects or the release of endothelial‐derived relaxant factor (EDRF). The inhibitory effects were reversed on prolonged washout, indicating that the effects were not due to destruction of the endothelial cells. 3 In superfusion experiments, palmitoyl carnitine inhibited the release of EDRF from rat aorta but did not affect the responsiveness to exogenous EDRF, indicating a site of action at the endothelial cell. In superfusion experiments, palmitoyl carnitine, and lysophosphatidyl choline, caused direct relaxations of the aorta, indicating EDRF release, prior to inhibition of release evoked by receptor stimulation. These substances may modulate vascular responsiveness under certain conditions.