TY - JOUR
T1 - Effect of taurine deficiency on adenosine receptor-mediated relaxation of the rat aorta
AU - Abebe, Worku
AU - Mozaffari, Mahmood S.
N1 - Funding Information:
The authors thank Champa Patel and Nehal Ahmmed for technical assistance. The work presented in this communication was supported by residual funds from a grant by Taisho Pharmaceutical Company of Japan (MSM).
PY - 2003/11
Y1 - 2003/11
N2 - 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 β-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 N6-cyclopentyladenosine (CPA). The adenosine analogs produced concentration-dependent (1×10-9-3×10-3 M) relaxations of aortas from both control and β-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 β-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 A2A 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 β-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 β-alanine treatment, suggesting that not only similar responses can be generated by a given adenosine agonist in different vascular beds, but also β-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.
AB - 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 β-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 N6-cyclopentyladenosine (CPA). The adenosine analogs produced concentration-dependent (1×10-9-3×10-3 M) relaxations of aortas from both control and β-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 β-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 A2A 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 β-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 β-alanine treatment, suggesting that not only similar responses can be generated by a given adenosine agonist in different vascular beds, but also β-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.
KW - Adenosine analogs
KW - Rat aorta
KW - Taurine deficiency
KW - Vasorelaxation
KW - β-Alanine
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U2 - 10.1016/j.vph.2003.08.001
DO - 10.1016/j.vph.2003.08.001
M3 - Article
C2 - 14746829
AN - SCOPUS:1642514531
SN - 1537-1891
VL - 40
SP - 219
EP - 228
JO - Vascular Pharmacology
JF - Vascular Pharmacology
IS - 4
ER -