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肾利钠降压系统在肾实质减少型高血压大鼠高血压机制中的作用

The role of renal natriuretic depressor systems on hypertensive mechanisms in reduced renal mass hypertensive rats.

作者信息

Shimamoto K, Ura N, Ishiguro T, Nakagawa M, Iimura O

机构信息

Second Department of Internal Medicine, Sapporo Medical University School of Medicine, Japan.

出版信息

Hypertens Res. 1995 Jun;18 Suppl 1:S53-7. doi: 10.1291/hypres.18.supplementi_s53.

Abstract

The pathophysiological role of renal natriuretic depressor systems and endogenous digitalis like factor (EDLF) on blood pressure (BP) elevation was studied in reduced renal mass rats (RRM) with saline loading for a model of volume dependent hypertension. Fifty-four male Sprague-Dawley rats were operated on to remove varying proportions of their kidney mass (5/6 RRM, n = 13; 4/6 RRM, n = 16; 3/6 RRM, n = 12) or sham operated (control, n = 13). They were given 1% saline to drink for 4 weeks. BP was elevated significantly at the 1st week in 5/6 RRM and continued to increase until the 4th week, but this was not seen in the other 3 groups. Urine volume (UV) and urinary sodium excretion (UNaV) increased after saline loading in all groups. Urinary kallikrein excretion was significantly lower in order of the 5/6, 4/6 and 3/6 RRM at the basal state and after saline loading. A significant negative correlation was observed between urinary kallikrein and BP. Urinary PGE2 was increased in each RRM in order of the 5/6, 4/6 and 3/6 RRM groups. A significant positive correlation was observed between urinary PGE2 and BP, UV or UNaV. The basal urinary DA excretion was significantly lower in 3 RRMs than in the control. After saline drinking, urinary DA increased in 3 RRMs, while differences disappeared in the control and RRMs. Urinary EDLF increased immediately after the initiation of saline loading in all groups, except the control group, and returned to the basal level 2 weeks later in 3/6 and 4/6 RRM. Only in 5/6 RRM, the urinary EDLF remained higher than the basal level.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

在肾质量减少大鼠(RRM)中,通过生理盐水负荷建立容量依赖性高血压模型,研究肾利钠降压系统和内源性洋地黄样因子(EDLF)对血压(BP)升高的病理生理作用。54只雄性Sprague-Dawley大鼠接受手术切除不同比例的肾脏(5/6肾切除,n = 13;4/6肾切除,n = 16;3/6肾切除,n = 12)或假手术(对照组,n = 13)。给它们饮用1%生理盐水4周。5/6肾切除组在第1周血压显著升高,并持续升高至第4周,但其他3组未见此现象。所有组在生理盐水负荷后尿量(UV)和尿钠排泄(UNaV)均增加。基础状态及生理盐水负荷后,尿激肽释放酶排泄量按5/6、4/6和3/6肾切除组顺序显著降低。尿激肽释放酶与血压之间存在显著负相关。尿PGE2在各肾切除组中按5/6、4/6和3/6肾切除组顺序增加。尿PGE2与血压、UV或UNaV之间存在显著正相关。3个肾切除组基础尿多巴胺排泄量显著低于对照组。饮用生理盐水后,3个肾切除组尿多巴胺增加,而对照组和肾切除组之间的差异消失。除对照组外,所有组在开始生理盐水负荷后尿EDLF立即增加,3/6和4/6肾切除组在2周后恢复至基础水平。仅在5/6肾切除组,尿EDLF仍高于基础水平。(摘要截断于250字)

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