Yuasa S, Sumikura T, Yura T, Takahashi N, Shoji T, Uchida K, Fujioka H, Miki S, Matsuo H, Takamitsu Y
Second Department of Internal Medicine, Kagawa Medical School, Japan.
Blood Press. 1996 Mar;5(2):121-7. doi: 10.3109/08037059609062118.
Dietary Ca is an important modulator of blood pressure in humans and rats. Since the kidney plays a key role in the pathogenesis of hypertension, the effects of a low Ca diet (0.01% Ca) on blood pressure and pressure natriuresis response were studied in normotensive Sprague-Dawley rats. In addition, a possible role of the renin-angiotensin system in the development of hypertension and an altered pressure natriuresis response resulting from low dietary Ca intake was examined. In the low Ca diet group, systolic blood pressure measured by the tail-cuff method was significantly higher than in the normal Ca diet group (1,1% Ca) 1 week after the diet (1 13.0 +/- 7.1 vs. 105.0 +/- 9.5mmHg, p < 0.05). After 4 weeks, the hypertension was more pronounced. Low dietary Ca intake significantly inhibited the water and sodium excretory responses to acute elevation of renal perfusion pressure by tightening an infrarenal aortic constriction. Treatment with an inhibitor of angiotensin-converting enzyme, captopril (30 mg/kg/day), completely abolished the elevation of blood pressure and attenuated the reduced pressure natriuresis response observed in Ca-deficient rats. Although plasma renin activity was not different between the low and normal Ca diet groups after the 2-week dietary regimen, the pressor response to angiotensin II was enhanced by 30% in the low Ca diet group and there was a significant difference in the pressor response between the two groups. These results suggest a possible involvement of the renin-angiotensin system in the development of hypertension and an inhibitory effect on the pressure natriuresis response caused by low dietary Ca intake, via an enhanced sensitivity to angiotensin II.
膳食钙是人类和大鼠血压的重要调节因子。由于肾脏在高血压发病机制中起关键作用，因此在正常血压的Sprague-Dawley大鼠中研究了低钙饮食（0.01%钙）对血压和压力性利钠反应的影响。此外，还研究了肾素-血管紧张素系统在高血压发展中的可能作用以及低钙饮食摄入导致的压力性利钠反应改变。在低钙饮食组中，采用尾套法测量的收缩压在饮食1周后显著高于正常钙饮食组（1.1%钙）（113.0±7.1 vs. 105.0±9.5mmHg，p<0.05）。4周后，高血压更为明显。低钙饮食摄入通过收紧肾下主动脉缩窄显著抑制了对肾灌注压急性升高的水和钠排泄反应。用血管紧张素转换酶抑制剂卡托普利（30mg/kg/天）治疗可完全消除血压升高，并减轻缺钙大鼠中观察到的压力性利钠反应降低。尽管在2周饮食方案后，低钙饮食组和正常钙饮食组之间的血浆肾素活性没有差异，但低钙饮食组对血管紧张素II的升压反应增强了30%，两组之间的升压反应存在显著差异。这些结果表明，肾素-血管紧张素系统可能参与高血压的发展，并通过增强对血管紧张素II的敏感性，对低钙饮食摄入引起的压力性利钠反应产生抑制作用。
