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两种盐敏感性诱导高血压大鼠模型中的血压、镁及其他矿物质平衡:1型非肽类血管紧张素II受体拮抗剂的作用

Blood pressure, magnesium and other mineral balance in two rat models of salt-sensitive, induced hypertension: effects of a non-peptide angiotensin II receptor type 1 antagonist.

作者信息

Rondón Lusliany Josefina, Marcano Eunice, Rodríguez Fátima, del Castillo Jesús Rafael

机构信息

Instituto Venezolano de Investigaciones Científicas (IVIC), Centro de Biofísica y Bioquímica, Laboratorio de Fisiología Molecular, Altos de Pipe, Estado Miranda, Venezuela.

IVIC, Centro de Química, Laboratorio de Química Analítica, Altos de Pipe, Estado Miranda, Venezuela.

出版信息

Magnes Res. 2014 Jul-Sep;27(3):113-30. doi: 10.1684/mrh.2014.0368.

DOI:10.1684/mrh.2014.0368
PMID:25560239
Abstract

The renin-angiotensin system is critically involved in regulating arterial blood pressure (BP). Inappropriate angiotensin type-1 receptor activation by angiotensin-II (Ang-II) is related to increased arterial BP. Mg has a role in BP; it can affect cardiac electrical activity, myocardial contractility, and vascular tone. To evaluate the relationship between high BP induced by a high sodium (Na) diet and Mg, and other mineral balances, two experimental rat models of salt-sensitive, induced-hypertension were used: Ang-II infused and Dahl salt-sensitive (SS) rats. We found that: 1) Ang-II infusion progressively increased BP, which was accompanied by hypomagnesuria and signs of secondary hyperaldosteronism; 2) an additive effect between Ang-II and a high Na load may have an effect on strontium (Sr), zinc (Zn) and copper (Cu) balances; 3) Dahl SS rats fed a high Na diet had a slow pressor response, accompanied by altered Mg, Na, potassium (K), and phosphate (P) balances; and 4) losartan prevented BP increases induced by Ang II-NaCl, but did not modify mineral balances. In Dahl SS rats, losartan attenuated high BP and ameliorated magnesemia, Na and K balances. Mg metabolism maybe considered a possible defect in this strain of rat that may contribute to hypertension.

摘要

肾素-血管紧张素系统在调节动脉血压(BP)方面起着关键作用。血管紧张素-II(Ang-II)对1型血管紧张素受体的不适当激活与动脉血压升高有关。镁在血压调节中发挥作用;它可以影响心脏电活动、心肌收缩力和血管张力。为了评估高钠(Na)饮食诱导的高血压与镁以及其他矿物质平衡之间的关系,我们使用了两种盐敏感性诱导高血压的实验大鼠模型:Ang-II灌注大鼠和Dahl盐敏感(SS)大鼠。我们发现:1)Ang-II灌注使血压逐渐升高,同时伴有低镁尿症和继发性醛固酮增多症的迹象;2)Ang-II与高钠负荷之间的叠加效应可能对锶(Sr)、锌(Zn)和铜(Cu)平衡产生影响;3)喂食高钠饮食的Dahl SS大鼠升压反应缓慢,同时伴有镁、钠、钾(K)和磷酸盐(P)平衡的改变;4)氯沙坦可预防Ang II-氯化钠诱导的血压升高,但不会改变矿物质平衡。在Dahl SS大鼠中,氯沙坦可减轻高血压并改善血镁、钠和钾平衡。镁代谢可能被认为是该品系大鼠中可能导致高血压的一个潜在缺陷。

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