The pathogenesis of hypertension: black-white differences.

Cardiovascular clinics Pub Date : 1991-01-01
M P Blaustein, C E Grim
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Abstract

In summary, for reasons that are not clear, some persons seem to be extremely good at retaining sodium on a high-sodium diet or poor at excreting sodium on a high-sodium intake. This is more frequent in Western hemisphere blacks than in whites in the West or in blacks in Africa. These geographic/ethnic differences in sodium handling ability may be related to environmental factors or, more likely, to inherited differences in the ability to conserve sodium based on the evolutionary principle of survival fo the fittest for the ability to conserve sodium. The frequency of this salt-conserving (thrifty) genotype in Western hemisphere blacks may have been further increased as a consequence of severe selection pressures for survival based on the ability to conserve sodium during the slavery period of history in the West. One characteristic of the blood pressure control systems of Western hemisphere blacks is suppression of plasma renin activity without suppression of aldosterone production. In addition there is greater nephrosclerosis in blacks than whites and a more rapid decline in creatinine clearance with age. When more sodium is ingested than the kidneys are able to handle (excrete), there is a (transient) slight positive sodium balance; as a result sodium, chloride, and water are retained, resulting in an expansion of plasma volume (Fig. 7-3). The initial physiologic responses include (increased) secretion of atrial natriuretic peptides and the digitalis-like substance (natriuretic hormone), and inhibition of vasopressin and aldosterone secretion. The net effect is directly enhanced natriuresis and diuresis, and a reduction in plasma volume, with no significant effect on blood pressure. However, if there is a continuing tendency to sodium retention and volume expansion, the capacity of the aforementioned mechanisms to control plasma volume will be exceeded; then, the chronically elevated level of the digitalis-like substance will inhibit the sodium pumps in the arterial and venous smooth muscle cells and in the sympathetic neurons. The increased venous tone will help to reduce plasma volume directly by reducing central venous volume. Arterial tone will be increased by direct action of the digitalis-like substance on the arterial smooth muscle and, indirectly, via the hormone's action on the sympathetic neurons. Initially, of course, blood pressure will be maintained in the normal range (but will be labile) because of the compensating cardiovascular reflexes. Once the capacity of these reflexes to control blood pressure is exceeded, however, the blood pressure will begin to rise; this will induce a pressure natriuresis to help restore plasma volume to normal.(ABSTRACT TRUNCATED AT 400 WORDS)

高血压的发病机制:黑白差异。
总之,由于不清楚的原因,有些人似乎在高钠饮食中非常善于保留钠,而在高钠饮食中却不善于排出钠。这在西半球的黑人中比在西方的白人或非洲的黑人中更常见。这些钠处理能力的地理/种族差异可能与环境因素有关,或者更有可能与基于适者生存以保存钠能力的进化原则的保存钠能力的遗传差异有关。在西半球黑人中,这种节约盐(节俭)基因型的频率可能进一步增加,这是由于在西方奴隶制历史时期,基于保存钠的能力,生存的严重选择压力的结果。西半球黑人血压控制系统的一个特点是抑制血浆肾素活性而不抑制醛固酮的产生。此外,黑人的肾硬化比白人更严重,随着年龄的增长,肌酐清除率下降得更快。当摄入的钠超过肾脏能够处理(排泄)的量时,会有一个(短暂的)轻微的正钠平衡;结果钠、氯化物和水被保留,导致血浆体积膨胀(图7-3)。最初的生理反应包括(增加)心房利钠肽和洋地黄样物质(利钠激素)的分泌,抑制抗利尿素和醛固酮的分泌。净效果是直接增强利钠和利尿,血浆量减少,对血压无显著影响。然而,如果钠潴留和体积膨胀的趋势持续,上述机制控制血浆体积的能力将被超越;然后,长期升高的洋地黄样物质会抑制动脉和静脉平滑肌细胞和交感神经元中的钠泵。静脉张力升高将通过减少中心静脉容量直接帮助减少血浆容量。动脉张力会通过地黄样物质对动脉平滑肌的直接作用和激素对交感神经元的间接作用而增强。当然,一开始,血压会维持在正常范围内(但会不稳定),因为补偿性心血管反射。然而,一旦这些反射控制血压的能力被超过,血压就会开始上升;这会引起压力尿钠,帮助血浆容量恢复正常。(摘要删节为400字)
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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