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儿茶酚胺在血管紧张素诱导的高血糖症中的作用。

Role of catecholamines in angiotensin induced hyperglycaemia.

作者信息

Singh K N, Agrawal S, Chandra V, Mittal R K

出版信息

Indian J Physiol Pharmacol. 1976 Jul-Sep;20(3):130-5.

PMID:977079
Abstract

The effects of angiotensin II were studied on blood sugar level in dogs. Intracerebroventricular administration of pressor dose of angiotensin caused a rise in blood sugar level. The hyperglycaemia and pressor response was not affected by bilateral vagotomy and was less marked in adrenalectomized dogs. The hyperglycaemic effect and pressor response was not observed in reserpinized and spinal vagotomized dogs. It is suggested that centrally administered angiotensin stimulates the hypothalamic or medullary accelerator neurons (central sympathetic structures) to cause a marked release of catecholamines from peripheral stores specially adrenal medulla. This excessive release of catecholamines is responsible for hyperglycaemia and pressor response of angiotensin II in dogs.

摘要

研究了血管紧张素II对犬血糖水平的影响。向脑室内注射升压剂量的血管紧张素会导致血糖水平升高。高血糖和升压反应不受双侧迷走神经切断术的影响,在肾上腺切除的犬中则不太明显。在利血平化和脊髓迷走神经切断的犬中未观察到高血糖效应和升压反应。提示中枢给予血管紧张素会刺激下丘脑或延髓的加速神经元(中枢交感结构),从而导致外周储存部位特别是肾上腺髓质大量释放儿茶酚胺。儿茶酚胺的这种过度释放是犬体内血管紧张素II引起高血糖和升压反应的原因。

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