Tabrizchi R
Division of Basic Medical Sciences, Faculty of Medicine, Memorial University of Newfoundland, St. John's, Canada.
Naunyn Schmiedebergs Arch Pharmacol. 1997 Jul;356(1):69-75. doi: 10.1007/pl00005030.
The effects of adenosine and adenosine analogues, 2-[p-(2-[carboxyethyl) phenethylamino]-5'-N-ethylcarboxamidoadenosine (CGS 21680) and N6-2-(4-aminophenyl)-ethyladenosine (APNEA), on mean arterial pressure, cardiac output, mean circulatory filling pressure, arterial resistance, venous resistance and heart rate in untreated or treated (with ganglion-blockers mecamylamine and atropine) pentobarbital-anesthetized rats were examined. Infusion of adenosine (100, 300 and 900 microg/kg/min), CGS 21680 (0.1, 0.3 and 0.9 microg/kg/min) or APNEA (1.0, 3.0 and 9.0 microg/kg/min) reduced mean arterial pressure and arterial resistance in all groups. Adenosine and APNEA also reduced mean circulatory filling pressure, venous resistance and heart rate in untreated animals. Furthermore, APNEA but not adenosine reduced cardiac output. In contrast, CGS 21680 increased cardiac output and heart rate but did not have any effect on mean circulatory filling pressure or venous resistance. In ganglion-blocked rats, APNEA reduced cardiac output, mean circulatory filling pressure and heart rate, while adenosine did not have any effect on these parameters. In addition, APNEA and adenosine reduced arterial resistance but were unable to alter venous resistance while CGS 21680 reduced mean circulatory filling pressure and arterial resistance but did not further affect cardiac output, heart rate and venous resistance in ganglion-blocked animals. The results of the present study suggest that adenosine and APNEA dilate arterioles and vein, whereas CGS 21680 causes arterial dilatation but not venodilatation in untreated animals due to hypotension-induced sympathetic activation. A possible explanation for the present observations could be differences in the distribution of vascular A2 versus A3 adenosine receptors in the venous circulation.
研究了腺苷及腺苷类似物2-[对-(2-羧乙基)苯乙氨基]-5'-N-乙基甲酰胺基腺苷(CGS 21680)和N6-2-(4-氨基苯基)乙基腺苷(APNEA)对未处理或经神经节阻滞剂美加明和阿托品处理的戊巴比妥麻醉大鼠平均动脉压、心输出量、平均循环充盈压、动脉阻力、静脉阻力和心率的影响。输注腺苷(100、300和900微克/千克/分钟)、CGS 21680(0.1、0.3和0.9微克/千克/分钟)或APNEA(1.0、3.0和9.0微克/千克/分钟)可降低所有组的平均动脉压和动脉阻力。腺苷和APNEA还可降低未处理动物的平均循环充盈压、静脉阻力和心率。此外,APNEA而非腺苷可降低心输出量。相比之下,CGS 21680可增加心输出量和心率,但对平均循环充盈压或静脉阻力无任何影响。在神经节阻断的大鼠中,APNEA可降低心输出量、平均循环充盈压和心率,而腺苷对这些参数无任何影响。此外,APNEA和腺苷可降低动脉阻力,但无法改变静脉阻力,而CGS 21680可降低神经节阻断动物的平均循环充盈压和动脉阻力,但对心输出量、心率和静脉阻力无进一步影响。本研究结果表明,在未处理的动物中,腺苷和APNEA可使小动脉和静脉扩张,而CGS 21680可导致动脉扩张但不导致静脉扩张,这是由于低血压诱导的交感神经激活所致。对目前观察结果的一种可能解释可能是静脉循环中血管A2与A3腺苷受体分布的差异。