Effect of taurine deficiency on adenosine receptor-mediated relaxation of the rat aorta

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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 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.

Original languageEnglish (US)
Pages (from-to)219-228
Number of pages10
JournalVascular Pharmacology
Volume40
Issue number4
DOIs
StatePublished - Jan 1 2003

Fingerprint

Purinergic P1 Receptors
Taurine
Aorta
Alanine
Endothelium
Adenosine
NG-Nitroarginine Methyl Ester
2-Chloroadenosine
Adenosine A2A Receptors
Superior Mesenteric Artery
varespladib methyl
Vasodilation
Blood Vessels
Nitric Oxide

Keywords

  • Adenosine analogs
  • Rat aorta
  • Taurine deficiency
  • Vasorelaxation
  • β-Alanine

ASJC Scopus subject areas

  • Physiology
  • Molecular Medicine
  • Pharmacology

Cite this

Effect of taurine deficiency on adenosine receptor-mediated relaxation of the rat aorta. / Abebe, Worku; Mozaffari, Mahmood S.

In: Vascular Pharmacology, Vol. 40, No. 4, 01.01.2003, p. 219-228.

Research output: Contribution to journalArticle

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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.

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