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OtherCARDIOVASCULAR PHARMACOLOGY

Effect of Low Density Lipoprotein on Adenosine Receptor-Mediated Coronary Vasorelaxation in Vitro

Worku Abebe and S. Jamal Mustafa
Journal of Pharmacology and Experimental Therapeutics August 1997, 282 (2) 851-857;
Worku Abebe
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S. Jamal Mustafa
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Abstract

We investigated the effect of low density lipoprotein (LDL) on vasorelaxations and nitric oxide generation induced by the adenosine analogs, 5′-(N-ethylcarboxamide)adenosine, 2-p-(2-carboxyethyl)phenylethyl-amino-5′N-ethylcarboxamidoadenosine and/or 2-chloroadenosine in porcine coronary artery rings in vitro. Preincubation of tissues with native LDL (100 and 200 μg/ml) for 4 hr in the absence or presence of copper sulfate (5 μM) selectively attenuated the endothelium-dependent relaxations elicited by 5′-(N-ethylcarboxamide)adenosine and 2-p-(2-carboxyethyl)phenylethyl-amino-5′N-ethylcarboxamideoadenosine without altering the response to 2-chloroadenosine which produced endothelium-independent relaxation. The 4-hr exposure of tissues to native LDL (100 μg/ml) also inhibited the production of nitrite induced by 5′-(N-ethylcarboxamide)adenosine in endothelium-intact rings. These effects were associated with enhanced oxidation of the lipoprotein. The inhibitory action of LDL on tissue relaxations and nitrite generation as well as the oxidation of the lipoprotein were all prevented by high density lipoprotein (100 μg/ml). In contrast, a relatively short period (20 min) of tissue incubation with native LDL produced no alterations of the relaxations and nitrite production evoked by 5′-(N-ethylcarboxamide)adenosine and 2-p-(2-carboxyethyl)phenylethyl-amino-5′N-ethylcarboxamidoadenosine. Under this condition, the oxidation of LDL was not also significantly altered. In conclusion, the results indicate that in coronary artery LDL, with oxidative modification, causes attenuation of nitric oxide-mediated endothelial responses induced by adenosine receptors activation, and this effect is prevented by high density lipoprotein. Such modulation may be of importance in hypercholesterolemia and in the development of atherosclerosis.

Footnotes

  • Send reprint requests to: Dr. S. Jamal Mustafa, Department of Pharmacology, School of Medicine, East Carolina University, Greenville, NC 27858.

  • ↵1 This work was supported by NHLBI Grant HL-27339 and a Research Supplement for Minority Individuals to W.A. (HL-50049).

  • Abbreviations:
    LDL
    low density lipoprotein
    n-LDL
    native LDL
    HDL
    high density lipoprotein
    NECA
    5′-(N-ethylcarboxamide)adenosine
    CGS-21680
    2-p-(2-carboxyethyl)phenylethyl-amino-5′N-ethylcarboxamidoadenosine
    CAD
    2-chloroadenosine
    TBARS
    thiobarbituric acid reactive substance
    MAD
    malondialdehyde
    PGF2α
    prostaglandin F2α
    o-LDL
    oxidatively modified LDL
    EC50
    50% of maximum relaxations
    • Received October 15, 1996.
    • Accepted April 7, 1997.
  • The American Society for Pharmacology and Experimental Therapeutics
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Journal of Pharmacology and Experimental Therapeutics
Vol. 282, Issue 2
1 Aug 1997
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OtherCARDIOVASCULAR PHARMACOLOGY

Effect of Low Density Lipoprotein on Adenosine Receptor-Mediated Coronary Vasorelaxation in Vitro

Worku Abebe and S. Jamal Mustafa
Journal of Pharmacology and Experimental Therapeutics August 1, 1997, 282 (2) 851-857;

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OtherCARDIOVASCULAR PHARMACOLOGY

Effect of Low Density Lipoprotein on Adenosine Receptor-Mediated Coronary Vasorelaxation in Vitro

Worku Abebe and S. Jamal Mustafa
Journal of Pharmacology and Experimental Therapeutics August 1, 1997, 282 (2) 851-857;
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