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兔尾侧腹外侧延髓 N-甲基-D-天冬氨酸受体阻断后的压力感受器-血管运动反射

Baroreceptor-vasomotor reflex after N-methyl-D-aspartate receptor blockade in rabbit caudal ventrolateral medulla.

作者信息

Blessing W W

机构信息

Department of Medicine, Flinders University of South Australia, Bedford Park.

出版信息

J Physiol. 1989 Sep;416:67-78. doi: 10.1113/jphysiol.1989.sp017749.

Abstract
  1. Experiments were performed in anaesthetized rabbits to determine whether blockade of N-methyl-D-aspartate receptors in the caudal ventrolateral medulla oblongata prevents the changes in renal sympathetic vasomotor activity which normally occur in response to increases or decreases in arterial pressure. 2. N-Methyl-D-aspartic acid receptor blockade using bilateral injections of either kynurenic acid (5 nmol) or DL-amino-5-phosphonovaleric acid (5 nmol) caused a rise in arterial pressure with a variable change in renal sympathetic nerve activity. 3. The depressor and renal sympathoinhibitory responses normally seen after intramedullary injection of N-methyl-D-aspartic acid (50 pmol) into the caudal ventrolateral medulla were entirely prevented by prior receptor blockade. The corresponding responses to L-glutamate (10 nmol) were not affected. 4. The depressor and renal sympathoinhibitory responses normally seen with electrical stimulation of the aortic depressor nerve were abolished by the receptor blockade. 5. The reflex inhibition of renal sympathetic nerve activity normally seen in response to increasing arterial pressure using a cuff around the descending aorta was not affected by kynurenic acid. The response was reduced by DL-amino-5-phosphonovaleric acid but a significant degree of inhibition was preserved. The reflex increase in renal sympathetic nerve activity normally seen in response to reducing arterial pressure using a cuff occluder around the inferior vena cava was unchanged after injection of DL-amino-5-phosphonovaleric acid and was increased in magnitude after injection of kynurenic acid. 6. The results indicate that blockade of excitatory amino acid receptors in the caudal ventrolateral medulla of the rabbit abolishes the depressor response evoked by electrical stimulation of the aortic nerve but leaves intact the normal baroreceptor-vasomotor responses elicited by raising or lowering arterial pressure.
摘要
  1. 在麻醉的兔子身上进行实验,以确定延髓尾端腹外侧部N-甲基-D-天冬氨酸受体的阻断是否能防止肾交感血管运动活性的变化,这种变化通常会随着动脉血压的升高或降低而发生。2. 双侧注射犬尿氨酸(5纳摩尔)或DL-氨基-5-磷酸缬氨酸(5纳摩尔)阻断N-甲基-D-天冬氨酸受体,导致动脉血压升高,肾交感神经活性发生变化。3. 在延髓尾端腹外侧部髓内注射N-甲基-D-天冬氨酸(50皮摩尔)后通常出现的降压和肾交感抑制反应,在预先进行受体阻断后完全被阻止。对L-谷氨酸(10纳摩尔)的相应反应未受影响。4. 受体阻断消除了电刺激主动脉减压神经时通常出现的降压和肾交感抑制反应。5. 使用围绕降主动脉的袖带增加动脉血压时,通常看到的肾交感神经活性的反射性抑制不受犬尿氨酸影响。DL-氨基-5-磷酸缬氨酸使该反应减弱,但仍保留显著程度的抑制。使用围绕下腔静脉的袖带阻塞器降低动脉血压时,通常看到的肾交感神经活性的反射性增加在注射DL-氨基-5-磷酸缬氨酸后未改变,在注射犬尿氨酸后幅度增加。6. 结果表明,阻断兔延髓尾端腹外侧部的兴奋性氨基酸受体会消除电刺激主动脉神经引起的降压反应,但不会影响通过升高或降低动脉血压引发的正常压力感受器-血管运动反应。

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