CAJ | 학술논문

目的：探讨高钠盐引发的高血压发病机制。方法：雄性SD大鼠40只，分为对照(NC)组、高盐(HS)组、高盐+L-精氨酸(HS+Arg)组、高盐+依那普利(HS+En)组和高盐+特拉唑嗪(HS+Ter)组，每组8只。各组饲料相同。NC组饮去离子水；HS组饮1.5%氯化钠溶液；HS+Arg组、HS+En组和HS+Ter组分别饮用1.5%氯化钠溶液配制的L-精氨酸(4g.kg-1.d-1)、依那普利(30mg.kg-1.d-1)和盐酸特拉唑嗪(4mg.kg-1.d-1)。第8周末，大鼠在戊巴比妥钠麻醉下，直接测量颈总动脉血压，开腹抽取下腔静脉血及剖取肾脏、肾上腺。测定前海葱苷原A样物质(PLC)水平，Na＋-K＋-ATP酶活性，NO(x)、内皮素(ET)及血管紧张素II(AngII)水平。结果：HS组大鼠血压显著高于NC组，血浆PLC、ET及肾上腺AngII水平皆显著高于NC组；血浆和肾组织NO(x)和AngII水平、肾脏Na＋-K＋-ATP酶活性皆明显低于NC组；HS+Arg组、HS+En组和HS+Ter组大鼠血压和血浆PLC水平皆显著低于HS组，血浆和肾组织NO(x)水平及Na＋-K＋-ATP酶活性皆明显高于HS组；HS+Arg组、HS+En组和HS+Ter组肾上腺AngII水平及HS+Arg组血浆ET水平明显低于HS组，并与NC组相近。结论：在高钠盐引发的高血压发病机制中，除钠泵抑制因子释放增加致细胞膜Na＋-K＋-ATP酶活性减低外，内皮功能损害致NO释放减少也可能起重要作用。
목적：탐토고납염인발적고혈압발병궤제。방법：웅성SD대서40지，분위대조(NC)조、고염(HS)조、고염+L-정안산(HS+Arg)조、고염+의나보리(HS+En)조화고염+특랍서진(HS+Ter)조，매조8지。각조사료상동。NC조음거리자수；HS조음1.5%록화납용액；HS+Arg조、HS+En조화HS+Ter조분별음용1.5%록화납용액배제적L-정안산(4g.kg-1.d-1)、의나보리(30mg.kg-1.d-1)화염산특랍서진(4mg.kg-1.d-1)。제8주말，대서재무파비타납마취하，직접측량경총동맥혈압，개복추취하강정맥혈급부취신장、신상선。측정전해총감원A양물질(PLC)수평，Na＋-K＋-ATP매활성，NO(x)、내피소(ET)급혈관긴장소II(AngII)수평。결과：HS조대서혈압현저고우NC조，혈장PLC、ET급신상선AngII수평개현저고우NC조；혈장화신조직NO(x)화AngII수평、신장Na＋-K＋-ATP매활성개명현저우NC조；HS+Arg조、HS+En조화HS+Ter조대서혈압화혈장PLC수평개현저저우HS조，혈장화신조직NO(x)수평급Na＋-K＋-ATP매활성개명현고우HS조；HS+Arg조、HS+En조화HS+Ter조신상선AngII수평급HS+Arg조혈장ET수평명현저우HS조，병여NC조상근。결론：재고납염인발적고혈압발병궤제중，제납빙억제인자석방증가치세포막Na＋-K＋-ATP매활성감저외，내피공능손해치NO석방감소야가능기중요작용。
AIM: To reveal the pathogenesis of salt-induced hypertension.METHODS: Forty male SD rats were divided into five groups, which received on same chow but different drink. Control(NC)group: deionized water; High salt(HS)group: 1.5% NaCl solution; L-arginine(HS+Arg)group: L-arginine(4 gmg.kg-1.d-1)in 1.5% NaCl solution; Enalapril (HS+En) group: enalapril (30 mg.kg-1.d-1) in 1.5% NaCl solution; Terazozin(HS+Ter)group: terazozin(4 mgmg.kg-1.d-1)in 1.5% NaCl solution. At the end of 8 weeks, rats were anesthetized with pentobarbital sodium. Blood pressure(BP)were recorded and blood were drawn from inferior vena cava and kidneys, adrenals were removed. NO(x),ET and AngII, Na＋-K＋-ATPase and proscillaridin-like compound(PLC)were assayed. RESULTS: BP, PLC and ET in plasma and AngII in adrenal were increased, NO(x)and AngII in plasma and kidney were decreased in HS group compared with NC group. CONCLUSION: High salt intake may induce hypertension in SD rats. In addition to the Na＋-K＋-ATPase activity was inhibited by increased sodium-pump inhibitors, NO release decrease may also play an important role in the pathogenesis of hypertension.