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甲状腺激素与肾素分泌。

Thyroid hormones and renin secretion.

作者信息

Ganong W F

出版信息

Life Sci. 1982;30(7-8):561-9. doi: 10.1016/0024-3205(82)90270-3.

DOI:10.1016/0024-3205(82)90270-3
PMID:7040892
Abstract

Circulating angiotensin is produced by the action of renin from the kidneys on circulating angiotensinogen. There are other renin-angiotensin systems in various organs in the body, and recent observations raise the intriguing possibility that angiotensin II is produced by a totally intracellular pathway in the juxtaglomerular cells, the gonadotrops of the anterior pituitary, neurons, in the brain, salivary duct cells, and neuroblastoma cells. Circulating angiotensin II levels depend in large part on the plasma concentration of angiotensinogen, which is hormonally regulated, and on the rate of renin secretion. Renin secretion is regulated by an intrarenal baroreceptor mechanism, a macula densa mechanism, angiotensin II, vasopressin, and the sympathetic nervous system. The increase in renin secretion produced by sympathetic discharge is mediated for the most part by beta-adrenergic receptors, which are probably located on the juxtaglomerular cells. Hyperthyroidism would be expected to be associated with increased renin secretion in view of the increased beta-adrenergic activity in this condition, and hypothyroidism would be associated with decreased plasma renin activity due to decreased beta-adrenergic activity. Our recent research on serotonin-mediated increases in renin secretion that depend on the integrity of the dorsal raphe nucleus and the mediobasal hypothalamus has led us to investigate the effect of the pituitary on the renin response to p-chloroamphetamine. The response is potentiated immediately after hypophysectomy, but 22 days after the operation, it is abolished. This slowly developing decrease in responsiveness may be due to decreased thyroid function.

摘要

循环中的血管紧张素是由肾脏产生的肾素作用于循环中的血管紧张素原而生成的。体内各器官还存在其他肾素 - 血管紧张素系统,最近的观察结果提出了一个有趣的可能性,即血管紧张素II是由近球细胞、腺垂体促性腺激素细胞、脑内神经元、唾液腺导管细胞和神经母细胞瘤细胞中的完全细胞内途径产生的。循环中的血管紧张素II水平在很大程度上取决于受激素调节的血管紧张素原的血浆浓度以及肾素分泌率。肾素分泌受肾内压力感受器机制、致密斑机制、血管紧张素II、血管加压素和交感神经系统调节。交感神经放电引起的肾素分泌增加大部分是由β - 肾上腺素能受体介导的,这些受体可能位于近球细胞上。鉴于甲状腺功能亢进时β - 肾上腺素能活性增加,预计会伴有肾素分泌增加;而甲状腺功能减退时,由于β - 肾上腺素能活性降低,血浆肾素活性会降低。我们最近关于5 - 羟色胺介导的肾素分泌增加(其依赖于中缝背核和下丘脑中间基底部的完整性)的研究,促使我们研究垂体对肾素对对氯苯丙胺反应的影响。垂体切除术后立即反应增强,但术后22天反应消失。这种反应性的缓慢下降可能是由于甲状腺功能减退所致。

相似文献

1
Thyroid hormones and renin secretion.甲状腺激素与肾素分泌。
Life Sci. 1982;30(7-8):561-9. doi: 10.1016/0024-3205(82)90270-3.
2
Pharmacological evidence that the sympathetic nervous system mediates the increase in secretion of renin produced by p-chloroamphetamine.药理学证据表明,交感神经系统介导了对氯苯丙胺引起的肾素分泌增加。
Neuropharmacology. 1984 Nov;23(11):1237-40. doi: 10.1016/0028-3908(84)90039-x.
3
Evidence that the mediobasal hypothalamus is involved in serotonergic stimulation of renin secretion.有证据表明,下丘脑内侧基底部参与了血清素对肾素分泌的刺激作用。
Neuroendocrinology. 1982;34(5):323-6. doi: 10.1159/000123321.
4
The renin-angiotensin system and the central nervous system.肾素-血管紧张素系统与中枢神经系统。
Fed Proc. 1977 Apr;36(5):1771-5.
5
Role of brain serotonergic pathways and hypothalamus in regulation of renin secretion.脑血清素能通路及下丘脑在肾素分泌调节中的作用。
Am J Physiol. 1987 Jul;253(1 Pt 2):R179-85. doi: 10.1152/ajpregu.1987.253.1.R179.
6
Evidence that serotonergic neurons in the dorsal raphe nucleus exert a stimulatory effect on the secretion of renin but not of corticosterone.中缝背核中5-羟色胺能神经元对肾素分泌有刺激作用,但对皮质酮分泌没有刺激作用的证据。
Brain Res. 1982 Mar 11;235(2):233-43. doi: 10.1016/0006-8993(82)91003-4.
7
Effect of hypophysectomy on dipsogenic stimuli: evidence for angiotensin supersensitivity.
Am J Physiol. 1986 Jul;251(1 Pt 2):R53-8. doi: 10.1152/ajpregu.1986.251.1.R53.
8
Neuroendocrine regulation of plasma angiotensinogen.血浆血管紧张素原的神经内分泌调节
Endocrinology. 1991 Aug;129(2):901-6. doi: 10.1210/endo-129-2-901.
9
Peptides and neurotransmitters that affect renin secretion.
J Hypertens Suppl. 1984 Oct;2(1):75-82.
10
Blood, pituitary, and brain renin-angiotensin systems and regulation of secretion of anterior pituitary gland.血液、垂体和脑肾素-血管紧张素系统与腺垂体分泌的调节。
Front Neuroendocrinol. 1993 Jul;14(3):233-49. doi: 10.1006/frne.1993.1008.

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