Sparks D P, Paul D J, Williams C A
Department of Physiology, College of Medicine, East Tennessee State University, Johnson City 37614.
Cardiovasc Res. 1987 Jul;21(7):521-9. doi: 10.1093/cvr/21.7.521.
The effects of clonidine, a central alpha 2 agonist, on changes in blood pressure caused by muscle afferent nerve (ergoreceptor) activation and baroreceptor manipulation were studied in cats. Prolonged isometric contractions (ergoreceptor activation) of the gastrocnemius and plantaris muscles increased mean arterial pressure by 53 mmHg. This pressor response was not altered by naloxone (0.5 mumol.litre-1) but was eliminated by clonidine (0.5-2.0 micrograms) when injected into the cerebral aqueduct. Brief occlusion of the carotid artery (15-30 s) caused mean arterial pressure to increase by 32-42 mmHg at rest. Neither naloxone nor clonidine altered the magnitude of the reflex pressor response to carotid occlusion. Similar increases in pressure were measured when occlusion was applied during fatiguing isometric contractions; thus baroreceptor induced increases in pressure were superimposed on the ergoreceptor induced blood pressure changes. Naloxone did not affect the changes in pressure caused by either reflex response. Clonidine continued to eliminate the pressor response to muscular contraction but did not affect the pressure increase when the carotid occlusion was applied during contractions. Electrical stimulation of the carotid sinus nerve caused blood pressure to decrease by 36 mmHg during rest and by 41 mmHg during fatiguing isometric contractions. Clonidine did not alter the depressor response to carotid sinus nerve stimulation. These data may indicate that separate pathways centrally mediate the changes in blood pressure caused by ergoreceptor and baroreceptor afferent activation. The integration of the ergoreceptor pathway may involve a catecholaminergic-opioidergic system but the present results do not suggest a similar interaction for the baroreceptor integration.
在猫身上研究了中枢性α2激动剂可乐定对肌肉传入神经（工作感受器）激活和压力感受器操作引起的血压变化的影响。腓肠肌和跖肌的长时间等长收缩（工作感受器激活）使平均动脉压升高53 mmHg。这种升压反应不受纳洛酮（0.5 μmol·升-1）影响，但向脑导水管注射可乐定（0.5 - 2.0微克）可消除该反应。短暂阻断颈动脉（15 - 30秒）在静息时使平均动脉压升高32 - 42 mmHg。纳洛酮和可乐定都未改变对颈动脉阻断的反射性升压反应幅度。在疲劳性等长收缩期间进行阻断时，测得的压力升高相似；因此，压力感受器诱导的压力升高叠加在工作感受器诱导的血压变化上。纳洛酮不影响任何一种反射反应引起的压力变化。可乐定继续消除对肌肉收缩的升压反应，但在收缩期间应用颈动脉阻断时不影响压力升高。电刺激颈动脉窦神经在静息时使血压降低36 mmHg，在疲劳性等长收缩期间使血压降低41 mmHg。可乐定未改变对颈动脉窦神经刺激的降压反应。这些数据可能表明，工作感受器和压力感受器传入激活引起的血压变化在中枢由不同途径介导。工作感受器途径的整合可能涉及儿茶酚胺能 - 阿片肽能系统，但目前的结果未提示压力感受器整合存在类似相互作用。
