Neuronal and vascular reactivity in isolated perfused kidneys during the development of spontaneous hypertension.

M G Collis, P M Vanhoutte
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引用次数: 9

Abstract

1. Vascular reactivity was studied in Tyrode solution perfused kidneys from young (7 weeks) and mature (4-6 months) spontaneously hypertensive rats (SH rats). 2. The response to nerve stimulation was greater in the kidneys from young SH rats than in those from young control rats, both in control solution and after inhibition of the disposition of noradrenaline; both groups exhibited the same sensitivity to noradrenaline, angiotensin II and barium chloride. 3. The response to nerve stimulation was normal in kidneys from mature SH rats, but responses to noradrenaline, angiotensin II and barium chloride were greater than the control. 4. Cocaine potentiated the response to nerve stimulation more in the kidneys from mature SH rats than in those from the control rats. 5. The results suggest that renal sympathetic nerves release more noradrenaline than normal in the young SH rats, which could be an important factor in causing hypertension. 6. In the established phase of spontaneous hypertension the vascular reactivity to exogenous agonists is increased, probably as a consequence of high blood pressure; the more efficient neuronal uptake causes normalization of the response to sympathetic nerve stimulation.

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自发性高血压发生过程中离体灌注肾的神经元和血管反应性。
1. 用Tyrode溶液灌注幼年(7周)和成年(4-6个月)自发性高血压大鼠(SH大鼠)肾脏,研究其血管反应性。2. 无论是在对照溶液中还是抑制去甲肾上腺素处置后,年轻SH大鼠肾脏对神经刺激的反应都比年轻对照大鼠大;两组对去甲肾上腺素、血管紧张素II和氯化钡的敏感性相同。3.成熟SH大鼠肾脏对神经刺激的反应正常,但对去甲肾上腺素、血管紧张素II和氯化钡的反应比对照大。4. 可卡因增强了成熟SH大鼠肾脏对神经刺激的反应,而不是对照大鼠。5. 结果提示,幼龄SH大鼠肾交感神经释放的去甲肾上腺素高于正常水平,这可能是引起高血压的重要因素。6. 在自发性高血压的既定阶段,血管对外源性激动剂的反应性增加,可能是高血压的结果;更有效的神经元摄取导致交感神经刺激反应正常化。
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Proceedings of the Fifth Meeting of the International Society of Hypertension, Paris, 12-14 June 1978. Brain catecholamines and catecholamine-synthesizing enzymes in renovascular hypertension in the rat. Enhanced hypothalamic noradrenaline biosynthesis in Goldblatt I renovascular hypertension. Definitive evidence for renin in rat brain by affinity chromatographic separation from protease. Renal release of active and inactive renin in essential and renovascular hypertension.
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