摘要
该文旨在用心房肽受体阻断剂（HS142—1．HS）研究对肾脏的作用，以探讨心房肽（ANP）受体在遗传性盐敏感Dahl大鼠（DS）是否存在缺陷。对DS及盐抵抗大鼠（DR）（各n＝8）分别高钠（8％NaCl）和正常钠（0．46％NaCl）饮食4周，麻醉状态下静注HS（10mg／kg），观察急性肾功能改变。结果：高钠饮食后，DS组血压明显上升而DR组不变。静注HS后DR组肾小球滤过率（GFR）、肾血流量（RPF）下降明显低于DS组（P均＜0．05），而肾血管阻力（RVR）明显升高（P＜0．05），排钠分数（FENa）下降也较明显。正常钠饮食4周后两组血压均正常，静注HS后DS组上述指标仍然不及DR组明显改变（P＜0．05）。结论：遗传性盐敏感高血压存在对内源性ANP减弱的GFR、RPF、RVR等肾血流动力学反应，可能参与钠，最终引起高血压的发病。
The aim of present study was to assess the effects of acute administration of HS 142 1 (HS), an antagonist of atrial natriuretc peptide(ANP) receptor on renal function and to determine whether there was a primary defect in intrarenal ANP receptor in Dahl salt-sensitive (DS) rats.Renal function was measured in anesthetized DS and resistant (DR) rats (aa n=8), receiving high or normal sodium diets for 4 weeks and after a bolus dose of HS (10mg/kg, i.v). In high sodium groups,glomerular filtration rate (GFR) and renal plasma flow rate (RPF) were markedly reduced and renal vascular resistance (RVR) increased in normotensive DR rats (respectively, P<0.05), but were not significantly changed in hypertensive DS rats. In normal sodimm diets both groups showed normal blood presure and similar changes in above parameters were found. Fractional sodium excretion (FENa) reduced more in DR rats than in DS rats after high sodium diet. These diminished responses of GFR, RPF and RVR to ANP receptor inhibition observed in DS rats, imply a defect of ANP receptor in the regulation of renal hemodynamic and excretory function which may be an important factor promoting sodium retention and ultimately the development of hypertension in DS rats.
出处
《上海第二医科大学学报》
CSCD
1997年第6期436-438,共3页
Acta Universitatis Medicinalis Secondae Shanghai
关键词
盐敏感性
高血压
肾功能
心房肽
受体阻滞剂
Dahl salt-sensitive rat
hypertension
renal function
atrial natriuretic peptide receptor antagonist
