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视前正中核的红藻氨酸损伤:对清醒大鼠中血管紧张素II诱导的饮水和升压反应的影响

Kainic acid lesions of the median preoptic nucleus: effects on angiotensin II induced drinking and pressor responses in the conscious rat.

作者信息

Jones D L

机构信息

Department of Physiology, University of Western Ontario, London, Canada.

出版信息

Can J Physiol Pharmacol. 1988 Aug;66(8):1082-6. doi: 10.1139/y88-176.

Abstract

Input to the nucleus medianus of the preoptic region has been suggested to be involved in both the drinking and pressor responses elicited by the central administration of angiotensin II. Evidence in support of this suggestion has been gained principally from electrical lesion experiments. This lesion procedure does not differentiate between the cells of the region and fibers coursing through the region. To test the hypothesis that cells in this region are involved in both the pressor and drinking responses elicited by central administration of angiotensin II, injections of kainic acid were made to induce lesions of the cells, while sparing fibers of passage. Drinking and blood pressure responses were determined pre- and post-lesion in the chronically instrumented awake rat. Injections of 50 ng angiotensin II in a 2-microL volume into a lateral cerebral ventricle of the conscious rat elicited pronounced drinking and pressor responses with a latency of 3-5 min. Lesions of the median preoptic region produced by injecting 1.0 microgram of kainic acid in 0.25 microL for 15 s attenuated or blocked the drinking response and increased the latency to drink induced by central injections of angiotensin II. However, kainic acid lesions did not significantly alter the pressor responses produced by angiotensin II administration. These results suggest that cells in the median preoptic region are involved in the drinking response but do not participate in the pressor response elicited by angiotensin II administration into a lateral cerebral ventricle of the conscious rat.

摘要

视前区正中核的传入神经被认为参与了中枢给予血管紧张素II所引发的饮水和升压反应。支持这一观点的证据主要来自电损伤实验。这种损伤方法无法区分该区域的细胞和穿过该区域的纤维。为了检验该区域的细胞参与中枢给予血管紧张素II所引发的升压和饮水反应这一假设,注射海人酸以诱导细胞损伤,同时保留通过的纤维。在长期植入仪器的清醒大鼠中,在损伤前后测定饮水和血压反应。向清醒大鼠的侧脑室注射体积为2微升、含50纳克血管紧张素II的溶液,引发明显的饮水和升压反应,潜伏期为3 - 5分钟。通过注射0.25微升含1.0微克海人酸的溶液持续15秒所造成的视前区正中核损伤,减弱或阻断了饮水反应,并延长了中枢注射血管紧张素II诱导的饮水潜伏期。然而,海人酸损伤并未显著改变血管紧张素II给药所产生的升压反应。这些结果表明,视前区正中核的细胞参与饮水反应,但不参与向清醒大鼠侧脑室注射血管紧张素II所引发的升压反应。

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