BRADYKININ CONTRIBUTES TO THE EXERCISE PRESSOR REFLEX - MECHANISM OF ACTION
BRADYKININ CONTRIBUTES TO THE EXERCISE PRESSOR REFLEX - MECHANISM OF ACTION
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DOI：
10.1152/jappl.1993.75.5.2061
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发表时间：
1993-11-01
影响因子：
3.3
通讯作者：
LONGHURST, JC
中科院分区：
文献类型：
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作者：
PAN, HL;STEBBINS, CL;LONGHURST, JC
本研究确定了负责介导缓激肽对引起麻醉猫升压反射的骨骼肌传入的作用的受体。在8只猫中，在静脉注射激肽B2受体拮抗剂（NPC 17731，20 μ g/kg）之前和之后，将1 μ g缓激肽动脉内注射到股薄肌中。最初注射缓激肽反射性地使平均动脉压增加23 +/- 7 mmHg，随时间推移的最大压力变化为439 +/- 272 mmHg/s，心率增加11 +/- 4次/min。类似地注射激肽B1受体激动剂des-Arg 9-缓激肽没有引起心血管反应（n = 6）。在8只不同的动物中，在激肽B2受体阻断后，平均动脉压、左心室压力随时间的最大变化以及对30 s电刺激后肢收缩的心率反应分别减弱了50 +/- 6、55 +/- 7和41 +/-8%。在其他8只动物中，用吲哚美辛（2.5-3 mg/kg iv）抑制前列腺素合成后，平均动脉压、左心室压随时间的最大变化和心率反应分别降低58 +/- 8、66 +/- 6和40 +/-12%，然后通过随后的B2受体阻断消除。这些数据表明，缓激肽有助于运动升压反射，通过其对位于肌肉传入神经末梢上的激肽B2受体的作用。这种缓激肽效应的大部分依赖于局部浓度的胰头素，其可以增强这种肽对肌肉传入神经末梢的刺激作用，并且可以通过激活激肽B2受体来增强。
This study determined the receptors responsible for mediating bradykinin's effect on skeletal muscle afferents that cause the pressor reflex in anesthetized cats. In eight cats, 1 mug of bradykinin was injected intra-arterially into the gracilis muscle before and after intravenous injection of a kinin B2-receptor antagonist (NPC 17731, 20 mug/kg). Initial injection of bradykinin reflexly increased mean arterial pressure by 23 +/- 7 mmHg, maximal change in pressure over time by 439 +/- 272 mmHg/s, and heart rate by 11 +/- 4 beats/min. The hemodynamic response to bradykinin was abolished by kinin B2-receptor blockade. Similar injection of the kinin B1-receptor agonist des-Arg9-bradykinin caused no cardiovascular responses (n = 6). In eight different animals, mean arterial pressure, maximal change in left ventricular pressure over time, and heart rate responses to 30 s of electrically stimulated hindlimb contraction were attenuated by 50 +/- 6, 55 +/- 7, and 41 +/- 8%, respectively, after kinin B2-receptor blockade. In eight other animals, mean arterial pressure, maximal change in left ventricular pressure over time, and heart rate responses were reduced by 58 +/- 8, 66 +/- 6, and 40 +/- 12%, respectively, after inhibition of prostaglandin synthesis with indomethacin (2.5-3 mg/kg iv) and were then abolished by subsequent B2-receptor blockade. These data suggest that bradykinin contributes to the exercise pressor reflex through its action on kinin B2 receptors located on the nerve endings of the muscle afferents. The majority of this bradykinin effect is dependent on local concentrations of prostaglandins that can augment the stimulating action of this peptide on muscle afferent nerve endings and that may be enhanced by activation of kinin B2 receptors.