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慢性自发性高血压大鼠生命周期中醛固酮、脱氧皮质酮、皮质酮及催乳素的变化

Aldosterone, deoxycorticosterone, corticosterone, and prolactin changes during the lifespan of chronically and spontaneously hypertensive rats.

作者信息

Iams S G, McMurthy J P, Wexler B C

出版信息

Endocrinology. 1979 May;104(5):1357-63. doi: 10.1210/endo-104-5-1357.

Abstract

Male and female spontaneously hypertensive rats (SHR), which develop hypertension spontaneously with maturation, were autopsied at select time intervals from weaning to 28 months. Their blood pressure began to rise steeply at 4--5 weeks, reaching a zenith of 180--240 mm Hg after 4 months. Elevated blood pressures were maintained in both sexes. After 20 months, the male SHR began to die of myocardial infarction and hypotensive crisis. Heart and adrenal gland weight increased progressively not only during the phase of rapidly rising blood pressure but also during the period of plateaued but sustained high blood pressure. RIA of plasma levels of aldosterone, deoxycorticosterone, corticosterone, and PRL, under both quiescent and mildly stressful conditions, demonstrated that the pituitary-adrenal axis of SHR progressively increases its propensity to respond to stress with maturation. This capacity to respond to stress was maintained despite the severe high blood pressure and the attainment of relative old age, i.e. 2 yr. An incremental change in circulating PRL, corticosterone, and aldosterone as early as 2 months of age, when blood pressure levels are beginning to rise, suggests that there may be some connection between the genetically programmed pathogenesis of the spontaneous hypertension and the progressively increasing (with age) sensitivity of the pituitary-adrenal axis to stress.

摘要

雄性和雌性自发性高血压大鼠(SHR)会随着成熟而自发患上高血压,在从断奶到28个月的特定时间间隔进行尸检。它们的血压在4至5周时开始急剧上升,4个月后达到180至240毫米汞柱的峰值。两性的血压均持续升高。20个月后,雄性SHR开始死于心肌梗死和低血压危机。心脏和肾上腺重量不仅在血压快速上升阶段逐渐增加,而且在血压稳定但持续处于高水平的时期也逐渐增加。在安静和轻度应激条件下,对血浆中醛固酮、脱氧皮质酮、皮质酮和催乳素水平进行放射免疫分析表明,SHR的垂体-肾上腺轴随着成熟而逐渐增加其对应激作出反应的倾向。尽管血压严重升高且已达到相对老龄(即2岁),但这种对应激的反应能力仍得以维持。早在2个月大时,即血压水平开始上升时,循环中的催乳素、皮质酮和醛固酮就出现了递增变化,这表明自发性高血压的基因编程发病机制与垂体-肾上腺轴对应激的敏感性(随年龄)逐渐增加之间可能存在某种联系。

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