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直立性低血压综合征中的α-肾上腺素能受体

Alpha-adrenergic receptors in orthostatic hypotension syndromes.

作者信息

Kafka M S, Polinsky R J, Williams A, Kopin I J, Lake C R, Ebert M H, Tokola N S

出版信息

Neurology. 1984 Aug;34(8):1121-5. doi: 10.1212/wnl.34.8.1121.

Abstract

Alpha-adrenergic receptor function was measured in platelets from patients with orthostatic hypotension and normotensive controls. Patients with idiopathic orthostatic hypotension (IOH) or multiple system atrophy (MSA) had more alpha-receptors than controls. Patients with IOH, but not MSA, produced less prostaglandin E1 (PGE1)-stimulated cyclic AMP (cAMP) than controls. Patients with sympathotonic orthostatic hypotension (SOH) were similar to controls in receptor number and cAMP production. The percent norepinephrine (NE) inhibition of PGE1-stimulated cAMP production was similar in patients and controls. An increase in alpha-receptor number may result from decreased peripheral NE secretion in IOH and MSA. Increased alpha-receptor number and decreased cAMP production, which accompany essential hypertension, may contribute to the supine hypertension of IOH, and an increase in alpha-receptor number may contribute to the supine hypertension of MSA. SOH patients appear to have no abnormalities of alpha-receptor function.

摘要

在体位性低血压患者和血压正常的对照者的血小板中测量了α-肾上腺素能受体功能。特发性体位性低血压(IOH)或多系统萎缩(MSA)患者的α受体比对照者更多。IOH患者而非MSA患者产生的前列腺素E1(PGE1)刺激的环磷酸腺苷(cAMP)比对照者少。交感神经性体位性低血压(SOH)患者在受体数量和cAMP产生方面与对照者相似。患者和对照者中去甲肾上腺素(NE)对PGE1刺激的cAMP产生的抑制百分比相似。α受体数量增加可能是由于IOH和MSA中外周NE分泌减少所致。与原发性高血压相伴的α受体数量增加和cAMP产生减少,可能导致IOH的卧位高血压,而α受体数量增加可能导致MSA的卧位高血压。SOH患者似乎没有α受体功能异常。

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