Pressure natriuresis and the renal control of arterial blood pressure

Ivy,; Bailey, Matthew A.

doi:10.1113/jphysiol.2014.271676

Cited by 132 publications

(119 citation statements)

References 102 publications

(97 reference statements)

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“…This “volume-loading” theory (Figure 1), sometimes referred to as the “autoregulation” theory, 28 also describes the sequence of events through which the phenomenon of “abnormal pressure natriuresis” is said to initiate and sustain salt-induced hypertension. 29–32 Most theories of salt-induced hypertension share two core tenets: 1) salt-sensitive subjects have a subnormal ability to excrete a salt load that causes them to retain more sodium than normal salt-resistant subjects, and 2) such an abnormally increased renal retention of sodium causes an abnormally large increase in cardiac output and thereby contributes importantly to the hemodynamic initiation of salt-induced increases in blood pressure. Here we challenge the validity of both these tenets.…”

Section: Introductionmentioning

confidence: 99%

Vasodysfunction That Involves Renal Vasodysfunction, Not Abnormally Increased Renal Retention of Sodium, Accounts for the Initiation of Salt-Induced Hypertension

et al. 2016

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Prevailing theory holds that abnormally large increases in renal salt retention and cardiac output are early pathophysiologic events mediating initiation of most instances of salt-induced hypertension. This theory has come under increasing scrutiny because it is based on studies that lack measurements of sodium balance and cardiac output obtained during initiation of salt-loading in proper normal controls, i.e., salt-resistant subjects with normal blood pressure. Here we make the case for a “vasodysfunction” theory for initiation of salt-induced hypertension: In response to an increase in salt intake, a subnormal decrease in total peripheral resistance that involves a subnormal decrease in renal vascular resistance, in the absence of abnormally large increases in sodium retention and cardiac output, is the hemodynamic abnormality that usually mediates initiation of salt-induced increases in blood pressure (BP). It is the failure to normally decrease vascular resistance in response to salt loading that enables a normal increase of cardiac output to initiate the salt-induced increase in blood pressure. This theory is based on the results of properly controlled studies which consistently demonstrate that in salt-sensitive subjects, salt-loading initiates increased BP through a hemodynamic mechanism that: 1) does not usually involve early increases in sodium retention and cardiac output greater than those which occur with salt-loading in normal controls, and 2) usually involves an early failure to decrease vascular resistance to the same extent as that observed during salt-loading in normal controls. Multiple mechanisms including disturbances in nitric oxide and sympathetic nervous system activity likely underlie this subnormal vasodilatory response to salt that usually precedes and initiates salt-induced hypertension.

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Section: Introductionmentioning

confidence: 99%

Vasodysfunction That Involves Renal Vasodysfunction, Not Abnormally Increased Renal Retention of Sodium, Accounts for the Initiation of Salt-Induced Hypertension

et al. 2016

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“…In addition, many endocrine factors such as the renin-angiotensinaldosterone system, nitric oxide, and prostaglandins can shift the pressure-natriuresis to higher or lower set points. There is also a good evidence that sodium handling by the distal segments of the nephron is critical to the regulation of sodium balance in relation to changes in BP and that other factors such as the sympathetic nervous system, a local intrarenal infl ammation, and the generation of reactive oxygen species (ROS) can modify the pressure-natriuresis relationship [ 16 ]. The contribution of the kidneys to the development of hypertension has been demonstrated nicely using cross-transplantation studies in animals.…”

Section: Role Of Kidneys In the Pathogenesis Of Essential Hypertensionmentioning

confidence: 97%

Pathophysiology of Hypertension

Burnier

Wuerzner

2015

Pathophysiology and Pharmacotherapy of Cardiovascular Disease

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Hypertension is a rather simple phenotype characterized by an increase in systemic blood pressure above an arbitrarily defi ned threshold. Yet, the mechanisms leading to the increase in blood pressure are extremely complex and involved a wide variety of neurohormonal, renal, metabolic, and vascular factors. The causes of hypertension differ substantially in young children, in middle-aged men and women, and in the elderly. In children, hypertension is often the appearance of a renal or endocrine disease, whereas in adults, the large majority of patients with hypertension have an essential hypertension, a denomination refl ecting that the mechanisms are not fully understood although some well-defi ned pathogenic factors have been described in patients with hypertension associated with diabetes mellitus, obesity, hyperaldosteronism, renovascular hypertension, or renal diseases. In the elderly, hypertension is strongly associated with factors leading to vascular aging and loss of arterial elasticity. The purpose of this chapter is to review the pathophysiology of hypertension in these different clinical situations in light of the recent literature.

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“…As blood pressure increases, glomerular and medullary perfusion return to normal levels and tubular ischaemia is reduced. At the same time, the flow elevation stimulates ATP and nitric oxide production in the vessels, which then improves sodium excretion (Ivy & Bailey ). In fact, blood pressure remains elevated as a result of the tubulointerstitial alterations mentioned above, whereas the pressure natriuresis slope is abated.…”

Section: Atp and Hypertensionmentioning

confidence: 99%

Purinergic receptors in tubulointerstitial inflammatory cells: a pathophysiological mechanism of salt‐sensitive hypertension

2015

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Recent studies have suggested that both the tubulointerstitial inflammatory cells and the activation of purinergic receptors integrate common mechanisms that result in salt-sensitive hypertension. The basis of this hypothesis is that renal endothelial cells release ATP in response to shear stress in the setting of hypertension. It has been demonstrated that the over-expression and activation of the P2X7, P2Y12 and P2X1 receptors favour the elevation of blood pressure induced by high-salt intake. In addition, the release of interleukins and inflammatory mediators in the tubulointerstitial area appears to be related to the activation of these receptors. Renal vasoconstriction and tubulointerstitial injury develop as a result, which increase sodium reabsorption by epithelial cells. Consistent with these effects, the reduction of tubulointerstitial inflammation caused by immunosuppressants, such as mycophenolate mofetil, prevents the development of salt-sensitive hypertension. Also, P2X7-receptor knockout mice develop minor renal injury when hypertension is induced via the administration of deoxycorticosterone acetate and a high-salt diet. In the setting of angiotensin II-induced hypertension, which is an early stage in the development of salt-sensitive hypertension, an acute blockade with the specific, non-selective P2 antagonist pyridoxalphosphate-6-azophenyl-2',4'-disulfonic acid prevented the renal vasoconstriction induced by angiotensin II. In addition, it normalized glomerular haemodynamics and restored sodium excretion to control values. These findings suggest that chronic administration of P2 purinergic antagonists may prevent the deleterious effects of purinergic receptors during the development of salt-sensitive hypertension.

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Pressure natriuresis and the renal control of arterial blood pressure

Cited by 132 publications

References 102 publications

Vasodysfunction That Involves Renal Vasodysfunction, Not Abnormally Increased Renal Retention of Sodium, Accounts for the Initiation of Salt-Induced Hypertension

Vasodysfunction That Involves Renal Vasodysfunction, Not Abnormally Increased Renal Retention of Sodium, Accounts for the Initiation of Salt-Induced Hypertension

Pathophysiology of Hypertension

Purinergic receptors in tubulointerstitial inflammatory cells: a pathophysiological mechanism of salt‐sensitive hypertension

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