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下丘脑-肾去甲肾上腺素能系统在钾的降压作用中的作用

Role of hypothalamic-renal noradrenergic systems in hypotensive action of potassium.

作者信息

Fujita T, Sato Y

机构信息

Fourth Department of Internal Medicine, University of Tokyo School of Medicine, Japan.

出版信息

Hypertension. 1992 Oct;20(4):466-72. doi: 10.1161/01.hyp.20.4.466.

Abstract

To clarify the role of the renal and hypothalamic noradrenergic systems in the antihypertensive actions of dietary potassium supplementation in salt-loaded spontaneously hypertensive rats (SHR), we measured systolic blood pressure and norepinephrine turnover, which was determined from the rate of decline of tissue norepinephrine concentration after the administration of alpha-methyl-p-tyrosine, in 5-week-old SHR or age-matched Wistar-Kyoto (WKY) rats eating normal-NaCl (0.66%) or high-NaCl (8%) diet with supplementation of 8% KCl. In WKY rats, neither high-sodium nor high-potassium diets had an effect on blood pressure with no change in renal or hypothalamic norepinephrine turnover. In SHR, however, salt loading accelerated the development of hypertension. Potassium supplementation did not affect blood pressure in normal-sodium SHR but attenuated the rise in blood pressure with salt loads. Correspondingly, renal norepinephrine turnover in SHR was increased compared with that of WKY rats, and salt loading further potentiated the increased turnover in the kidney; however, no changes in hypothalamic turnover occurred. Potassium supplementation attenuated the rise in blood pressure with salt loads and the increased renal turnover. Stimulation of sympathetic discharge by cold exposure after the administration of alpha-methyl-p-tyrosine produced marked depletion of norepinephrine in most tissues. The loss of norepinephrine was significantly greater in both kidney and hypothalamus of salt-loaded SHR than in those of normal-sodium SHR, but potassium could normalize this. Thus, potassium not only diminished the increased renal norepinephrine turnover in the kidney under normal conditions but also attenuated the augmented renal and hypothalamic norepinephrine turnover by cold stress in salt-loaded SHR.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

为了阐明肾和下丘脑去甲肾上腺素能系统在盐负荷自发性高血压大鼠(SHR)饮食补钾降压作用中的作用,我们测量了5周龄SHR或年龄匹配的Wistar-Kyoto(WKY)大鼠的收缩压和去甲肾上腺素周转率,后者通过给予α-甲基-对-酪氨酸后组织去甲肾上腺素浓度的下降速率来确定,这些大鼠食用正常氯化钠(0.66%)或高氯化钠(8%)饮食,并补充8%氯化钾。在WKY大鼠中,高钠和高钾饮食对血压均无影响,肾或下丘脑去甲肾上腺素周转率也无变化。然而,在SHR中,盐负荷加速了高血压的发展。补钾对正常钠盐SHR的血压无影响,但减轻了盐负荷引起的血压升高。相应地,与WKY大鼠相比,SHR的肾去甲肾上腺素周转率增加,盐负荷进一步增强了肾脏中增加的周转率;然而,下丘脑周转率没有变化。补钾减轻了盐负荷引起的血压升高和肾周转率的增加。给予α-甲基-对-酪氨酸后冷暴露刺激交感神经放电,导致大多数组织中的去甲肾上腺素显著耗竭。盐负荷SHR的肾脏和下丘脑去甲肾上腺素的损失明显大于正常钠盐SHR,但钾可以使其恢复正常。因此,钾不仅在正常情况下减少了肾脏中增加的肾去甲肾上腺素周转率,而且在盐负荷SHR中减轻了冷应激引起的肾脏和下丘脑去甲肾上腺素周转率的增加。(摘要截短于250字)

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