The time course of salt-induced hypertension, and why it matters

Abstract

The epidemiology of salt-induced hypertension has been explored in detail in animal studies, in some cases involving exposures to excess dietary salt for much of the animal's lifespan. The results of these studies demonstrate the presence of two distinct time courses of the blood pressure response to a high salt intake: an acute (rapid) blood pressure response occurring over days to weeks, and a slow and progressive blood pressure response that develops over extremely long periods of time, amounting to a significant fraction of the lifespan in normal individuals. The acute form of salt sensitivity is well known in humans, having often been demonstrated as a fall in blood pressure during the period of salt restriction. The slow and progressive form of salt sensitivity has been demonstrated directly in rats and chimpanzees and is also evident in analyses of human cross-population data as a salt dependency of age-associated changes of blood pressure. This slow and progressive component of salt-induced hypertension may be attributable, at least in part, to a progressive rise in the acute salt sensitivity of blood pressure during sustained exposure to high salt. However, a progressively irreversible or 'self sustaining' component of salt-induced hypertension has also been demonstrated in rat studies. This irreversible component has not been completely characterized, but its presence raises the possibility that blood pressure responses to salt restriction may not fully reveal the contribution of salt to blood pressure or the epidemiology of hypertension. These various components of salt sensitivity (acute vs slow, reversible vs irreversible) should be considered in any comprehensive explanation of the effects of salt on blood pressure and especially in experimental studies of the genetic and physiological mechanisms underlying salt-induced hypertension.

Dietary Sodium and Cardiovascular Disease Risk — Measurement Matters

“…4,6–9 The effects of excess sodium intake on blood pressure can be both short-term and cumulative and long-lasting, in keeping with the higher prevalence of hypertension among older people, as shown in meta-analyses and global observational studies such as INTERSALT. 3,58,59 In addition, physiological studies in animals and humans indicate that sodium reduction could reduce cardiovascular risk through mechanisms independent of blood pressure, such as improved endothelial functioning, decreased arterial stiffness, and decreased left ventricular mass. 60 …”

A maternal high salt diet disturbs cardiac and vascular function of offspring

“…High dietary salt intake is an environmental factor linked with increased blood pressure and cardiovascular and renal injury [41,45]. A variety of mechanisms have been suggested to contribute to salt induced changes in blood pressure and cardiovascular function.…”

A multi-component model of the dynamics of salt-induced hypertension in Dahl-S rats

“…At the other extreme, high dietary salt intakes have also been demonstrated to affect BP on a much slower time scale of many months or years [9-12]. In some studies, these slow and progressive effects of salt have been found to be partly irreversible [13-15], the irreversible characteristic corresponding with a shift of the chronic pressure natriuresis relationship to higher BP levels [13,14]. Finally, an effect of sustained salt loading to alter the slope of the chronic pressure natriuresis relationship, amounting to a salt induced worsening of acute salt-sensitivity, has also been suggested [13,14].…”