SODIUM AND CALCIUM METABOLISM IN PREHYPERTENSIVE STATE

近年来，大量的兴趣集中在 钠、钙在高血压发病中的作用。 然而，将钠摄入与糖尿病的发生联系起来的证据 在人和实验动物中， 尽管有足够的说服力，但对于它的作用仍然存在严重的怀疑。 钙代谢的异常是导致 高血压 目前最被接受的假设是 钠摄入量高血压是人类受试者的易感因素 或者动物有遗传缺陷， 肾脏排泄钠负荷;这导致钠潴留 以及体液因子（利钠因子？） 这 最终导致高血压的发生。 摄入高钠摄入量并不是一个必要条件， 自发性高血压患者高血压的发生发展 大鼠（SHR），但它通过刺激高血压 交感神经系统 联系机制 钙代谢异常的成因和 高血压的发展仍不清楚。 而且 增加膳食营养素的肥胖效应的机制 SHR的钙摄入量尚未阐明。 有可能 钙可影响交感神经系统活动， 因此，血压。 在这项研究建议中要检验的假设是， 实验性高血压钠代谢异常 大鼠继发于交感神经过度活跃 系统（SNS）和钙平衡的改变可能会影响 血压通过SNS的行动。 为了验证这些假设 计划在SHR中使用WKY进行以下一系列实验 作为对照的大鼠：1）研究SNS刺激对 高血压前期肾神经活动与肾钠代谢 SHR; 2）交感神经抑制对肾钠的影响 在高血压前期SHR中的处理; 3）研究以确定是否 钙代谢的异常发生在 高血压的发展以及是否增加饮食 钙通过抑制SNS降低血压。

In recent years a great deal of interest has been focused on the role of sodium and calcium in the pathogenesis of hypertension. Whereas the evidence linking sodium ingestion to the genesis of hypertension in both man and in experimental animals is sufficiently convincing, serious doubts still remain as to the role of abnormalities in calcium metabolism in the genesis of hypertension. The most current accepted hypothesis linking sodium intake to hypertension is that predisposed human subjects or animals have a genetic defect involving the ability of the kidneys to excrete a sodium load; this leads to sodium retention and to stimulation of humoral factors (natriuretic factors?) which are ultimately responsible for the development of hypertension. Ingestion of high sodium intake is not a condition sine qua non for the development of hypertension in spontaneously hypertensive rats (SHR), but it aggravates hypertension through stimulation of the sympathetic nervous system. The mechanisms linking abnormalities in calcium metabolism to the genesis and development of hypertension remain unclear. Moreover, the mechanisms of the hypotensive effect of increased dietary calcium intake in SHR are not elucidated. It is possible that calcium may affect sympathetic nervous system activity and consequently, blood pressure. The hypothesis to be tested in this research proposal are that the abnormality in sodium metabolism in experimentally hypertensive rats is secondary to hyperactivity of the sympathetic nervous system (SNS) and that alterations in calcium balance may affect blood pressure through action on SNS. To test these hypothesis the following series of experiments are planned in SHR using WKY rats as controls: 1) studies on the effect of SNS stimulation on renal nerve activity and renal sodium handling in pre-hypertensive SHR; 2) effect of sympathetic nerve inhibition on renal sodium handling in pre-hypertensive SHR; 3) studies to determine whether abnormalities in calcium metabolism precede or follow the development of hypertension and whether increased dietary calcium lowers blood pressure through inhibition of SNS.