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  • Title: Effect of taurine deficiency on adenosine receptor-mediated relaxation of the rat aorta.
    Author: Abebe W, Mozaffari MS.
    Journal: Vascul Pharmacol; 2003 Nov; 40(4):219-28. PubMed ID: 14746829.
    Abstract:
    We recently demonstrated that chronic taurine supplementation or deficiency causes alterations in reactivity of the rat aorta to several vasoactive agents. In the present investigation, we examined the effects beta-alanine-induced endogenous taurine deficiency on the mechanical responsiveness of the isolated rat aorta to adenosine receptor stimulation with 2-chloroadenosine (CAD), 5'-N-ethylcarboxyamidoadenosine (NECA), and N(6)-cyclopentyladenosine (CPA). The adenosine analogs produced concentration-dependent (1 x 10(-9)-3 x 10(-3) M) relaxations of aortas from both control and beta-alanine-treated rats with the rank order of potencies NECA>CAD>CPA, which was consistent with A(2) receptor identification. CAD and NECA induced both endothelium-dependent and -independent relaxations of the aortas. The endothelium-dependent responses to both agents and the independent responses to CAD were significantly attenuated by beta-alanine treatment. The relaxation responses of the aortas from control and taurine-deficient rats to CAD and NECA were markedly antagonized by ZM241385 (10(-5) M), suggesting the involvement of A(2A) adenosine receptors. Further, N-nitro-L-arginine methyl ester (L-NAME; 10(-5) M) significantly attenuated the endothelium-mediated relaxation produced by CAD and NECA in both groups. However, the inhibitory effect of L-NAME was less on the beta-alanine-treated tissues, providing evidence that the effect of taurine deficiency was linked to a reduction in nitric oxide generation. As in the aorta, CAD produced both endothelium-dependent and -independent relaxation responses in the rat superior mesenteric artery, and both responses were inhibited by chronic beta-alanine treatment, suggesting that not only similar responses can be generated by a given adenosine agonist in different vascular beds, but also beta-alanine treatment modulates these responses. On the other hand, while CPA elicited only endothelium-independent aortic relaxation, this response was not altered by taurine deficiency. The results indicate that endogenous taurine deficiency causes differential inhibitory effects on adenosine receptor-mediated vasorelaxation, depending upon the agonists used. Given the recognized role of adenosine in the vasculature, these alterations suggest taurine-mediated modulation of blood flow regulation.
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