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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Coexisting independent sodium-sensitive and sodium-insensitive mechanisms of genetic hypertension in spontaneously hypertensive rats (SHR).
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Coexisting independent sodium-sensitive and sodium-insensitive mechanisms of genetic hypertension in spontaneously hypertensive rats (SHR).

机译：自发性高血压大鼠（SHR）中遗传性高血压同时存在的独立的钠敏感和钠敏感机制。

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Some essential hypertensive patients and genetic hypertensive rat strains have less than the normal levels of Mg2+ tightly bound to the plasma membranes of their erythrocytes and other cells, i.e., the magnesium binding defect (MgBD). This binding defect appears to cause increased passive permeability of the membrane to Na+ and thereby its increased intracellular concentration, particularly if the Na+-extrusion enzyme systems of the cell are also defective. The Na+-Ca2+ exchange system in the cell membrane exports Na+ and imports Ca2+, increasing the tone of the smooth muscle cell and thus producing hypertension (HTn). This HTn is Na+-sensitive. Evidence supporting this postulate was obtained by determining the intraerythrocyte total concentrations of Na+, Ca2+, K+, and Mg2+ in two strains of spontaneously hypertensive rats (SHR and SS/Jr rats, having the MgBD together with the other requisites of the Na+-sensitive pathway) and their respective controls (WKY and SR/Jr rats, in which this complete pathway is absent). The Na+ and Ca2+ concentrations in the hypertensive rats were increased, and that of K+ was decreased. The concentrations of these cations were very similar in the two hypertensive strains. The level of membrane tightly bound Ca2+ in SHR erythrocyte membranes was significantly higher than those in the other three rat strains, which were not statistically different from each other. These results support previously reported evidence of the existence of a novel HTn-generating mechanism in the SHR rat, in which the intracellular Ca2+ concentration is increased as the result of the enhanced diffusion of this ion into the cell and the accompanying deficiency of the Ca2+ extrusion enzyme systems. This pathway is therefore Na+-insensitive, i.e., Ca2+-sensitive.
机译：一些原发性高血压患者和遗传性高血压大鼠品系的Mg2 +含量低于正常水平，这些水平与他们的红细胞和其他细胞的质膜紧密结合，即镁结合缺陷（MgBD）。这种结合缺陷似乎引起膜对Na +的被动渗透性增加，从而引起其细胞内浓度增加，特别是如果细胞的Na +挤出酶系统也有缺陷。细胞膜中的Na + -Ca2 +交换系统输出Na +并输入Ca2 +，从而增加了平滑肌细胞的张力，从而产生了高血压（HTn）。该HTn对Na +敏感。通过确定两种自发性高血压大鼠（SHR和SS / Jr大鼠，具有MgBD以及其他Na +敏感途径的必需品）中红细胞内Na +，Ca2 +，K +和Mg2 +的总血红蛋白浓度，可以证明这一假设。 ）和它们各自的对照（WKY和SR / Jr大鼠，其中没有完整的途径）。高血压大鼠的Na +和Ca2 +浓度升高，而K +的浓度降低。在两个高血压菌株中，这些阳离子的浓度非常相似。 SHR红细胞膜中与Ca2 +紧密结合的膜水平显着高于其他三只大鼠品系，两者在统计学上没有差异。这些结果支持先前报道的证据，表明在SHR大鼠中存在新的HTn生成机制，其中该离子向细胞内扩散的增强和伴随的Ca2 +挤出不足导致细胞内Ca2 +浓度增加。酶系统。因此，该途径对Na +不敏感，即对Ca 2+不敏感。

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