Maintaining Balance Under Pressure

McDonough, Alicia A.; Nguyen, Mien T. X.

doi:10.1161/hypertensionaha.115.04593

Cited by 40 publications

(26 citation statements)

References 59 publications

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“…The simple explanation for this finding is extreme ENaC activation driving inappropriate Na + reabsorption during AngII infusion – with or without K + supplementation – necessitating hypertension to drive pressure natriuresis. 5 …”

Section: Discussionmentioning

confidence: 99%

“…In brief, we found that AngII increases abundance and stimulates transporters beyond the macula densa including the apically expressed cortical Na,K-2Cl cotransporter (NKCC2), 4 NCC and both cortical and medullary ENaC, while the resultant hypertension depresses the abundance and activation of cortical and medullary Na-H exchanger (NHE3), and medullary NKCC2. 5 In rodent models that exhibit blunted hypertensive responses to AngII, transporter profiling reveals blunting of either distal transporter activation and/or proximal transporter inhibition. 6–8 Even so, a direct association between distal co-transporter abundance and hypertension is not evident in mice overexpressing NCC, indicating the importance of integrating multiple mechanisms along the entire nephron.…”

Section: Introductionmentioning

confidence: 99%

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Potassium Supplementation Prevents Sodium Chloride Cotransporter Stimulation During Angiotensin II Hypertension

et al. 2016

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Ang II hypertension increases distal tubule Na-Cl cotransporter (NCC) abundance and phosphorylation (NCCp), as well as epithelial Na+ channel (ENaC) abundance and activating cleavage. Acutely raising plasma [K+] by infusion or ingestion provokes a rapid decrease in NCCp that drives a compensatory kaliuresis. The first aim tested whether acutely raising plasma [K+] with a single 3 hr 2% potassium meal would lower NCCp in Sprague Dawley rats after 14 days of AngII (400 ng/kg/min). The potassium-rich meal neither decreased NCCp nor increased K+ excretion. AngII infused rats exhibited lower plasma [K+] versus controls (3.6 ± 0.2 vs. 4.5 ± 0.1 mmol/L, p < 0.05) suggesting that Ang II mediated ENaC activation provokes K+ depletion. The second aim tested whether doubling dietary potassium intake from 1% (A1K) to 2% (A2K) would prevent K+ depletion during AngII infusion and, thus, prevent NCC accumulation. A2K fed rats exhibited normal plasma [K+] and 2-fold higher K+ excretion and plasma [aldosterone] versus A1K. In A1K rats, NCC, NCCpS71, and NCCpT53 abundance increased 1.5- to 3-fold versus controls (p< 0.05). The rise in NCC and NCCp abundance was prevented in the A2K rats, yet blood pressure did not significantly decrease. ENaC subunit abundance and cleavage increased 1.5- to 3-fold in both A1K and A2K; ROMK abundance was unaffected by Ang II or dietary K+. In summary, the accumulation and phosphorylation of NCC seen during chronic AngII infusion hypertension is likely secondary to potassium deficiency driven by ENaC stimulation.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Potassium Supplementation Prevents Sodium Chloride Cotransporter Stimulation During Angiotensin II Hypertension

et al. 2016

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“…53–55 However, these investigators 1, 3–5 and others 1, 2, 6, 8, 10–15 contend that in cases in which the hypertension is induced by increased salt intake, (e.g., reduced renal mass models of salt-sensitivity or spontaneous forms of salt-sensitivity), salt-sensitive subjects do undergo greater salt-induced increases in sodium balance and blood volume than normal. Yet, the results of acute and chronic studies in humans and animals consistently demonstrate that in normal salt-resistant subjects, the salt-induced increases in sodium retention, blood volume, and cardiac output are similar to, or greater than, those in salt-sensitive subjects.…”

Section: In Salt-sensitive Subjects Substantial Increases In Blood Vmentioning

confidence: 99%

“…1 Further, the results of appropriately controlled studies indicate that salt-induced hypertension is not usually initiated and maintained by the occurrence of greater sodium retention, volume expansion, and increases in cardiac output in salt-sensitive subjects than in salt-loaded normal subjects. 21, 23–25, 29–32, 41, 45, 46, 49, 50 Nevertheless, many investigators 1, 2, 6, 10–15 seek to align the results of contemporary genetic, immunologic, and other studies of salt-induced hypertension with traditional views on the mechanisms of salt-resistance and salt-sensitivity. The current observations suggest that it might be more useful to align such contemporary research findings with hypotheses 19, 70–74 which do not hold that normal subjects are resistant to salt-induced hypertension because they undergo little or no increase in sodium balance or blood volume in response to a high salt diet.…”

Section: Implications For the Pathogenesis Of Salt-induced Hypertensionmentioning

confidence: 99%

“…8 This view is incorporated, in full or in part, into many contemporary accounts of how various genetic, immunologic, and other factors determine acute or chronic blood pressure responses to a high salt intake. 1, 2, 6, 8, 10–15 In addition, Lifton and others have proposed that in the general population, genetic variants associated with decreased activity of sodium transporters in the renal tubule, contribute to resistance from hypertension by promoting increased salt excretion and decreased external salt balance. 16–18 …”

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confidence: 99%

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An alternative hypothesis to the widely held view that renal excretion of sodium accounts for resistance to salt-induced hypertension

Kurtz

DiCarlo

Pravenec

et al. 2016

Kidney International

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It is widely held that in response to high salt diets, normal individuals are acutely and chronically resistant to salt-induced hypertension because they rapidly excrete salt and retain little of it so that their blood volume, and therefore blood pressure, does not increase. Conversely, it is also widely held that salt-sensitive individuals develop salt-induced hypertension because of an impaired renal capacity to excrete salt that causes greater salt retention and blood volume expansion than that which occurs in normal salt-resistant individuals. Here we review results of both acute and chronic salt-loading studies that have compared salt-induced changes in sodium retention and blood volume between normal subjects (salt-resistant normotensive controls) and salt-sensitive subjects. The results of properly controlled studies strongly support an alternative view: during acute or chronic increases in salt intake, normal salt-resistant subjects undergo substantial salt retention and do not excrete salt more rapidly, retain less sodium, or undergo lesser blood volume expansion than do salt-sensitive subjects. These observations: 1) directly conflict with the widely held view that renal excretion of sodium accounts for resistance to salt-induced hypertension, and 2) have implications for contemporary understanding of how various genetic, immunologic, and other factors determine acute and chronic blood pressure responses to high salt diets.

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The Influence of Celery (Apium graveolens) Juice on Hypertension

Illes,

Rodrigues

2023

Reference Series in Phytochemistry

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Maintaining Balance Under Pressure

Cited by 40 publications

References 59 publications

Potassium Supplementation Prevents Sodium Chloride Cotransporter Stimulation During Angiotensin II Hypertension

Potassium Supplementation Prevents Sodium Chloride Cotransporter Stimulation During Angiotensin II Hypertension

An alternative hypothesis to the widely held view that renal excretion of sodium accounts for resistance to salt-induced hypertension

The Influence of Celery (Apium graveolens) Juice on Hypertension

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