α,β-methylene ATP elicits a reflex pressor response arising from muscle in decerebrate cats
α,β-methylene ATP elicits a reflex pressor response arising from muscle in decerebrate cats
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DOI：
10.1152/japplphysiol.00237.2002
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发表时间：
2002-09-01
影响因子：
3.3
通讯作者：
Kaufman, MP
中科院分区：
文献类型：
--
作者：
Hanna, RL;Hayes, SG;Kaufman, MP
在某种程度上，运动加压反射被认为是由化学刺激引起的，表明运动肌肉的血液供应不足以满足其新陈代谢需求。有证据表明，三磷酸腺苷或腺苷可能作为这些化学刺激之一发挥作用。例如，这两种物质的肌肉间质浓度在运动过程中都会增加。这一发现使我们检验了一种假设，即在去大脑的未麻醉猫的延髓动脉注射刺激P2X受体的α，β-亚甲基ATP(5，20和50µg/kg)和刺激P1受体的2-氯腺苷(25µg/kg)，会引起反射性升压反应。我们发现，动脉注射两种最高剂量的α，β-亚甲基三磷酸腺苷可引起升压反应，而动脉注射2-氯腺苷则不能。此外，切断坐骨神经或动脉注射选择性P2受体拮抗剂磷酸吡哆醛-6-偶氮苯基-2‘，4’-二磺酸(10 mg/kg)可阻断α，β-亚甲基ATP引起的升压反应。我们得出结论，刺激P2受体，可通过骨骼肌的血管供应获得，唤起反射性升压反应。此外，我们的发现与P2受体的刺激包含了引起运动加压反射的代谢错误信号的一部分的假设是一致的。
In part, the exercise pressor reflex is believed to be evoked by chemical stimuli signaling that blood supply to exercising muscles is not adequate to meet its metabolic demands. There is evidence that either ATP or adenosine may function as one of these chemical stimuli. For example, muscle interstitial concentrations of both substances have been found to increase during exercise. This finding led us to test the hypothesis that popliteal arterial injection of alpha, beta-methylene ATP (5, 20, and 50 mug/kg), which stimulates P2X receptors, and 2-chloroadenosine (25 mug/kg), which stimulates P1 receptors, evokes reflex pressor responses in decerebrate, unanesthetized cats. We found that popliteal arterial injection of the two highest doses of alpha, beta-methylene ATP evoked pressor responses, whereas popliteal arterial injection of 2-chloroadenosine did not. In addition, the pressor responses evoked by alpha, beta-methylene ATP were blocked either by section of the sciatic nerve or by prior popliteal arterial injection of pyridoxal phosphate-6-azophenyl-2',4'-disulfonic acid (10 mg/kg), a selective P2-receptor antagonist. We conclude that the stimulation of P2 receptors, which are accessible through the vascular supply of skeletal muscle, evokes reflex pressor responses. In addition, our findings are consistent with the hypothesis that the stimulation of P2 receptors comprises part of the metabolic error signal evoking the exercise pressor reflex.