期刊
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
卷 280, 期 5, 页码 H2329-H2335出版社
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpheart.2001.280.5.H2329
关键词
cerebral blood flow; parenchymal arteriole; CGS-21680; ZM-241385; adenosine receptors
资金
- NINDS NIH HHS [NS-30305, NS-21076] Funding Source: Medline
The purpose of this study was to investigate the receptor subtypes that mediate the dilation of rat intracerebral arterioles elicited by adenosine. Penetrating arterioles were isolated from the rat brain, cannulated with the use of a micropipette system, and luminally pressurized to 60 mmHg. Both adenosine and the A(2A) receptor-selective agonist CGS-21680 induced dose-dependent vasodilation (-logEC(50): 6.5 +/- 0.2 and 8.6 +/- 0.3, respectively). However, adenosine, which is capable of activating both A(2A) and A(2B) receptors, caused a greater maximal dilation than CGS-21680. The A(2A) receptor-selective antagonist ZM-241385 (0.1 mM) only partially inhibited the dilation induced by adenosine but almost completely blocked CGS-21680-induced dilation. Neither 8-cyclopentyl-1,3-dipropylxanthine (0.1 muM), an A(1) receptor-selective antagonist, nor MRS-1191 (0.1 muM), an A(3) receptor-selective antagonist, attenuated adenosine dose responses. Moreover, ZM-241385 had no effect on the dilation induced by ATP (10 muM) or acidic (pH 6.8) buffer. We concluded that the A(2A) receptor subtype mediates adenosine-induced dilation of intracerebral arterioles in the rat brain. Furthermore, our results suggest that A(2B) receptors may also participate in the dilation response to adenosine.
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