The Effect of Atrial Natriuretic Factor on Blood Pressure, Heart Rate, and Renal Functions in Conscious, Spontaneously Hypertensive Rats
The Effect of Atrial Natriuretic Factor on Blood Pressure, Heart Rate, and Renal Functions in Conscious, Spontaneously Hypertensive Rats
复制标题
心房钠尿因子对清醒自发性高血压大鼠血压、心率和肾功能的影响
作者：
M. Gellai;R. DeWolf;L. Kinter;R. Beeuwkes
心房利钠因子是由心房肌细胞释放的多肽，可能在控制血压、调节肾脏盐分和水的排泄中发挥作用。我们的研究旨在评估一种名为心房肽II的合成肽对清醒自发性高血压大鼠和正常血压Wistar-京都大鼠的血压和心率、肾脏血流动力学以及盐和水排泄的作用。5只自发性高血压大鼠和5只大鼠静脉注射心房肽II(0.1、1.0、10、10 0μg/kg)后，记录平均动脉压和心率的变化。在第二组大鼠中，以两种不同的剂量注入多肽90分钟：低剂量，1μg/kg+2μg/kg/hr；高剂量，10μg/kg+20μg/kg/hr。团注心房肽II导致高血压大鼠的平均动脉压呈剂量依赖性下降，但在正常血压大鼠中没有；心率保持不变。在持续注射两种剂量的心房肽II期间，血压逐渐下降，与Wistar-京都株相比，自发性高血压株表现出更高的敏感性。在大剂量注射期间，两个品系的心率都有所下降；这种下降只在高血压大鼠中显著。小剂量的心房肽II增加了两种模型大鼠的游离水清除率；钠排泄仅在高血压大鼠中增加。在两个菌株中，大剂量的心房肽II与一过性钠尿、肾小球滤过率无变化以及有效肾血流量减少有关。这些结果1)表明自发性高血压大鼠对心钠素的降压作用更敏感，2)不支持肾小球滤过率增加是心房肽作用的先决条件的假说，3)提示心房肽II对清醒大鼠肾脏水和钠的排泄可能有单独的和剂量依赖的作用。
Atrial natriuretic factors, polypeptides released by atrial myocytes, may play a role in the control of blood pressure and the regulation of renal salt and water excretion. Our studies were designed to assess the role of a synthetic peptide, atriopeptin II, on blood pressure and heart rate, renal hemodynamics, and salt and water excretion in conscious, spontaneously hypertensive rats and in normotensive Wistar-Kyoto rats. Changes in mean arterial pressure and heart rate were recorded following intravenous bolus injections (0.1, 1.0, 10, 100 μg/kg) of atriopeptin II in 5 spontaneously hypertensive and 5 Wistar-Kyoto rats. In a second group of rats the peptide was infused for 90 minutes in two different doses: low dose, 1 μg/kg + 2 μg/kg/hr; and high dose, 10 μg/kg + 20 μg/kg/hr. Bolus injections of atriopeptin II resulted in dose-dependent decreases in mean arterial pressure in the hypertensive, but not in the normotensive, rats; heart rates remained unchanged. Blood pressure decreased gradually during the sustained infusion of both doses of atriopeptin II, with the spontaneously hypertensive strain showing increased sensitivity compared to the Wistar-Kyoto strain. Heart rate decreased in both strains during infusion of the high dose; the decrease was significant only in the hypertensive rats. The low dose of atriopeptin II increased the clearance of free water in both strains of rate; sodium excretion was increased only in the hypertensive rats. The high-dose atriopeptin II was associated with transient natriuresis, unaltered glomerular filtration rate, and decreased effective renal blood flow in both strains. These results 1) show increased sensitivity of spontaneously hypertensive rats to the hypotensive action of atrial natriuretic factor, 2) do not support the hypothesis that an increased glomerular filtration rate is a prerequisite to the natriuretic effect of atrial peptide, and 3) suggest that atriopeptin II may exert separate and dose-dependent effects on renal water and sodium excretion in conscious rats.