α,β-methylene ATP elicits a reflex pressor response arising from muscle in decerebrate cats

被引:51
作者
Hanna, RL [1 ]
Hayes, SG
Kaufman, MP
机构
[1] Univ Calif Davis, Dept Internal Med, Div Cardiovasc Med, TB 172, Davis, CA 95616 USA
[2] Univ Calif Davis, Dept Human Physiol, Div Cardiovasc Med, Davis, CA 95616 USA
关键词
purines; exercise; autonomic nervous system; thin fiber muscle afferents; metabolic error signal;
D O I
10.1152/japplphysiol.00237.2002
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
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.
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页码:834 / 841
页数:8
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