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目的 :探讨长期摄入高钠盐饮食引发高血压的机理。方法 :以普通饲料和 1.5 % Na Cl溶液饲喂雄性 Sprague-Dawley大鼠 6周 ,颈动脉插管直接测量血压 ,EL ISA检测血浆中、肾上腺和下丘脑组织中哇巴因样物质 (oubain- likecom pound,OL C)和前海葱苷原 A样物质 (proscillaridin- likecom pound,PL C)免疫反应性 ,在有和无哇巴因存在的条件下水解 ATP测定 Na+ - K+ - ATP酶活性。结果 :高血压组动脉血压较对照组明显升高 (P<0 .0 0 1) ,体重、肾重、肾重 /体重比率、血浆中及肾上腺和下丘脑组织中OL C和 PL C水平分别明显高于对照组 (P<0 .0 0 1) ,肾脏Na+ - K+ - ATP酶活性明显低于对照组 (P<0 .0 0 1)。结论 :长期摄入高钠盐饮食可能通过体液容量扩张刺激肾上腺和下丘脑分泌 OL C和 PL C入血循环 ,抑制组织细胞特别是血管平滑肌细胞膜 Na+ - K+ - ATP酶活性 ,引起细胞内 Na+和游离 Ca2 +浓度升高而导致血压升高。
Objective: To investigate the mechanism of long-term intake of high sodium salt-induced hypertension. Methods: Male Sprague-Dawley rats were fed with normal diet and 1.5% NaCl solution for 6 weeks. The blood pressure was measured by carotid artery cannulation. The oubain-like substances in plasma, adrenal gland and hypothalamus were detected by ELISA. likecom pound (OLC), and proscarridin - likecom pound (PLc) immunoreactivity, and the activity of Na + - K + - ATPase was determined by hydrolyzing ATP in the presence and absence of ouabain. Results: The arterial blood pressure in hypertension group was significantly higher than that in control group (P <0.01). The body weight, kidney weight, kidney weight / body weight ratio, OL C and PL C levels in plasma and in adrenal gland and hypothalamus were (P <0.01), and the activity of Na + - K + - ATPase in kidney was significantly lower than that in the control group (P <0.01). CONCLUSION: Long - term intake of high sodium diet may stimulate the secretion of OL C and PL C from the adrenal gland and hypothalamus into the blood circulation through body fluid volume expansion, and inhibit Na + - K + - ATPase activity of tissue cells, especially vascular smooth muscle cells, causing intracellular Na + and free Elevated Ca2 + causes high blood pressure.