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- W145108794 abstract "This chapter discusses comparative aspects of salt and hypertension. The link between arterial pressure, sodium, and renal function is not just a matter of disease: fundamentally, the kidney is the main long-term regulator of arterial pressure, and it does so by sharply accelerating sodium excretion when pressure increases. Thus, salt loads are harmlessly excreted through a transient and mild elevation of arterial pressure, which leads to pressure natriuresis, or so the theory goes. It is noticeable, however, that the supporting data relate to extremely high salt intakes, whereas other experiments—also in dogs—show that such increases are associated with chronic expansion of extracellular fluid (ECF) volume and elevation of arterial pressure. The effects of sodium retention are not simply those of an expanded ECF volume but probably secondary effects on intracellular sodium, especially in arterioles. Sodium may also influence arterial pressure through changes in catecholamine secretion. In hypertension, the blunted pressure natriuresis causes an increased arterial pressure, which is adaptive in the sense that it overcomes the impaired sodium excretion and maintains sodium output." @default.
- W145108794 created "2016-06-24" @default.
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- W145108794 date "1995-01-01" @default.
- W145108794 modified "2023-09-23" @default.
- W145108794 title "Comparative Aspects of Salt and Hypertension" @default.
- W145108794 doi "https://doi.org/10.1016/b978-0-08-040842-2.50012-9" @default.
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