Low-calcium diet increases blood pressure and alters peripheral but not central angiotensin II binding sites in rats.
Low-calcium diet increases blood pressure and alters peripheral but not central angiotensin II binding sites in rats.
复制标题
低钙饮食会增加大鼠的血压并改变外周血管紧张素 II 结合位点，但不会改变中枢血管紧张素 II 结合位点。
DOI：
10.1097/00004872-198905000-00012
复制
发表时间：
1989
影响因子：
4.9
通讯作者：
Speth,RC
中科院分区：
文献类型：
--
作者：
Baksi,SN;Abhold,RH;Speth,RC
结肠癌;低钙饮食导致高血压的机制尚不清楚。从4周龄开始，我们研究了雄性Sprague-Dawley大鼠分别饲喂低钙（0.005% Ca; 0.5% P）和正常钙（1.4% Ca）饮食8周后，血管紧张素II （Ang II）受体在脑、肾上腺和膀胱中的结合情况。用125l-肌氨酸-异亮氨酸- 8 Ang II （125I-SI Ang II）饱和等温结合法测定下丘脑-丘脑-中隔（HTS）、肾上腺和膀胱平滑肌的Ang II受体位点。采用尾袖法每2周测定一次收缩压。在献祭时测定血清总Ca、Na+、K+醛固酮和Ang II以及骨密度和矿物质含量。慢性缺钙大鼠血压升高，膀胱平滑肌Ang II受体密度降低，肾上腺Ang II受体有增加的趋势。缺钙大鼠血清钙、骨密度和矿物质含量显著降低，而血清Na+升高。8周饮食方案后血清Ang II和醛固酮未发生变化。本文讨论了减少膳食钙摄入与肾素-血管紧张素-醛固酮系统有关的高血压作用的可能机制。
colon; The mechanism by which low-calcium (Ca) diet causes hypertension is unknown. We investigated angiotensin II (Ang II) receptor binding in brain, adrenals and urinary bladders in male Sprague-Dawley rats pair-fed a low-Ca (0.005% Ca; 0.5% P) and normal-Ca (1.4% Ca) diet for 8 weeks beginning at 4 weeks of age. The Ang II receptor sites in hypothalamus-thalamus-septum (HTS), adrenal glands and urinary bladder smooth muscle were measured by saturation isotherm binding using 125l-sarcosine1isoleucine8 Ang II (125I-SI Ang II). Systolic blood pressure was determined at 2-week intervals by tailcuff method. Serum total Ca, Na+, K+ aldosterone and Ang II and bone density and mineral content were determined at the time of sacrifice. Chronic Ca deficiency in rats raised blood pressure and decreased Ang II receptor density in bladder smooth muscles and tended to increase adrenal Ang II receptors. Serum Ca, bone density and mineral content were significantly lower in the Ca-deficient rats, while serum Na+ was elevated in this group. Serum Ang II and aldosterone were unaltered after the 8-week dietary regimen. Possible mechanisms for the hypertensive actions of reduced dietary Ca intake involving the renin-angiotensin-aldosterone system are discussed.