Katoh Y, Umemura S, Sugimoto K, Tomiyama M, Abe Y, Hirawa N, Ishii M
Second Department of Internal Medicine, Yokohama City University School of Medicine, Japan.
Jpn Heart J. 1998 Jan;39(1):109-19. doi: 10.1536/ihj.39.109.
This study compared renal and intestinal handling of sodium in Dahl-Iwai salt-sensitive (S) and salt-resistant (R) rats given a normal-salt diet (0.3% NaCl) and a high-salt diet (4.0% NaCl). Six-week-old female S and R rats (n = 7 each) were given a normal-salt diet for 14 days followed by a high-salt diet for 3 weeks. Systolic blood pressure was significantly higher in the S rats than in the R rats only at the end of the high-salt diet period (170 +/- 5, mean +/- SEM, vs 152 +/- 1 mmHg, p < 0.01). Daily sodium intake, water intake, urine volume, and urinary and fecal excretions did not significantly differ between the R and the S rats during the normal- and high-salt diets, except for a slight, although significant, decrease in fecal sodium excretion in the S rats as compared with the R rats in the 2nd week of the high-salt diet period. After switching from the normal-salt diet to the high-salt diet, urinary sodium excretion increased by 17- to 18-fold and fecal sodium excretion increased by about 5-fold in the 1st week of salt loading. The changes in urinary and fecal sodium excretions did not differ significantly between the groups. Cumulative sodium retention was similar in the two groups. The aldosterone/creatinine ratio in 24-hr urine, which was significantly lower in the S than in the R rats during the normal-salt diet, decreased to similar levels in both groups after salt loading, indicating a blunted response of aldosterone in the S rats. Thus, there were no discernible differences in renal and intestinal handling of sodium between the S and the R rats, except for a slight, but significant, difference in fecal sodium excretion in the 2nd week of the high-salt period. The results indicate that inappropriate suppression of aldosterone or some other mechanism induced by salt loading may be involved in blood pressure elevation in Dahl-Iwai S rats.
本研究比较了给予正常盐饮食（0.3%氯化钠）和高盐饮食（4.0%氯化钠）的达尔-岩井盐敏感（S）大鼠和盐抵抗（R）大鼠的肾脏和肠道对钠的处理情况。六周龄雌性S和R大鼠（每组n = 7）先给予正常盐饮食14天，随后给予高盐饮食3周。仅在高盐饮食期结束时，S大鼠的收缩压显著高于R大鼠（170±5，均值±标准误，对比152±1 mmHg，p < 0.01）。在正常盐和高盐饮食期间，R大鼠和S大鼠的每日钠摄入量、饮水量、尿量以及尿和粪便排泄量均无显著差异，只是在高盐饮食期的第2周，与R大鼠相比，S大鼠的粪便钠排泄量略有下降，尽管差异显著。从正常盐饮食转换为高盐饮食后，在盐负荷的第1周，尿钠排泄量增加了17至18倍，粪便钠排泄量增加了约5倍。两组之间尿和粪便钠排泄量的变化无显著差异。两组的累积钠潴留相似。在正常盐饮食期间，S大鼠24小时尿中醛固酮/肌酐比值显著低于R大鼠，盐负荷后两组该比值降至相似水平，表明S大鼠的醛固酮反应迟钝。因此，除了在高盐期第2周粪便钠排泄存在轻微但显著的差异外，S大鼠和R大鼠在肾脏和肠道对钠的处理方面没有明显差异。结果表明，盐负荷诱导的醛固酮不适当抑制或其他一些机制可能与达尔-岩井S大鼠的血压升高有关。
