Abnormal relation of extracellular fluid volume and exchangeable sodium with systemic arterial pressure in early borderline essential hypertension

Lebel, Marcel; Grose, John H.; Blais, R.

doi:10.1016/s0002-9149(84)80078-8

Cited by 10 publications

(3 citation statements)

References 21 publications

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“…The primary regulator of blood pressure is the kidney [8,9,62], by its ability to regulate salt balance. However, extracellular fluid volume and exchangeable Na + are not decreased in subjects with borderline hypertension and young hypertensive patients [63,64]. This apparent paradox can be explained by the temporal development of hypertension.…”

Section: Discussionmentioning

confidence: 99%

A linear relationship between the ex-vivo sodium mediated expression of two sodium regulatory pathways as a surrogate marker of salt sensitivity of blood pressure in exfoliated human renal proximal tubule cells: The virtual renal biopsy

Gildea

Lahiff

Sciver

et al. 2013

Clinica Chimica Acta

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Background Salt sensitivity (SS) of blood pressure (BP) affects 25% of adults, shares comorbidity with hypertension, and has no convenient diagnostic test. We tested the hypothesis that urine-derived exfoliated renal proximal tubule cells (RPTCs) could diagnose the degree of an individual's SS of BP. Methods Subjects were selected who had their SS of BP determined 5 y prior to this study (salt-sensitive: ≥7 mm Hg increase in mean arterial pressure (MAP) following transition from a random weekly diet of low (10 mmol/day) to high (300 mmol/day) sodium (Na+) intake, N = 4; inverse salt-sensitive (ISS): ≥7 mm Hg increase in MAP transitioning from a high to low Na+ diet, N = 3, and salt-resistant (SR): <7 mm Hg change in MAP transitioned on either diet, N = 5). RPTC responses to 2 independent Na+ transport pathways were measured. Results There was a negative correlation between the degree of SS and dopamine-1 receptor (D1R) plasma membrane recruitment (y = −0.0107x + 0.68 relative fluorescent units (RFU), R2 = 0.88, N = 12, P < 0.0001) and angiotensin II-stimulated intracellular Ca++ (y = −0.0016x + 0.0336, R2 = 0.7112, P < 0.001, N = 10) concentration over baseline. Conclusions Isolating RPTCs from urine provides a personalized cell-based diagnostic test of SS index that offers advantages over a 2-week controlled diet with respect to cost and patient compliance. Furthermore, the linear relationship between the change in MAP and response to 2 Na+ regulatory pathways suggests that an individual's RPTC response to intracellular Na+ is personalized and predictive.

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Section: Discussionmentioning

confidence: 99%

A linear relationship between the ex-vivo sodium mediated expression of two sodium regulatory pathways as a surrogate marker of salt sensitivity of blood pressure in exfoliated human renal proximal tubule cells: The virtual renal biopsy

Gildea

Lahiff

Sciver

et al. 2013

Clinica Chimica Acta

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“…Recently, Levy et al [28] have detected an insulin resistance in F344. F344 and borderline hypertensive patient exhibit high baseline plasma renin activity [29,30], and the lower fall in BP of F344 compared with SD rats in response to a b-agonist, showed by Caputo et al [6], also seems to be observed in borderline hypertension [31,32]. However, unlike sodium-resistant borderline hypertensive subjects whose large artery compliance is not altered [33], results of the present study suggest a structural modification of arterial wall in F344 which would rather lead to a reduced compliance.…”

Section: Discussionmentioning

confidence: 99%

Different vascular responsiveness to angiotensin II in two normotensive rat strains

Herin

Blanc

Basset

et al. 2003

Fundamemntal Clinical Pharma

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Rats of the Fischer 344 (F344) and Wistar Kyoto (WKY) strains are known to present differences in stimuli responses involving the renin-angiotensin system and in cardiovascular responses to an acoustic startle stimulus. Here we compared the vascular reactivity to angiotensin II (ANG II) of these normotensive, inbred rat strains. Blood pressure (BP) and heart rate (HR) were recorded in conscious rats, before and after a neurohumoral blockade obtained by successive administration of chlorisondamine, enalapril, a V1-vasopressinergic receptor antagonist (Manning compound) and atropine methyl nitrate. BP was restored by a constant infusion of noradrenaline. Boluses of ANG II ranging from 0.001 to 1280 ng/kg were injected randomly. Average dose-response curves were established. After neurohumoral blockade, the minimum mean BP (MBP) produced by hydralazine (3 mg/kg, i.v.) and the maximum MBP produced by noradrenaline (60 microg/mL and 800 microL/min, i.v.) were used to reflect arterial wall structure. The maximal systolic blood pressure (SBP) and pulse pressure (PP) responses to ANG II were higher in F344 compared with WKY (+86 +/- 3 mmHg vs. +71 +/- 3 mmHg, P < 0.01 for SBP, +31 +/- 2 mmHg vs. +18 +/- 1 mmHg, P < 0.001 for PP). After the ANG II type 1 (AT1) receptor blocker valsartan, ANG II had no significant effect on BP. F344 and WKY exhibited the same maximum MBP in response to noradrenaline. However, MBP level following hydralazine was higher in F344 (F344: 48 +/- 2 mmHg vs. WKY: 37 +/- 3 mmHg, P < 0.01). The amplification in F344 of the vasoconstrictive response to ANG II mediated by AT1 receptors is compatible with a high number of AT1 receptors in this strain. In F344, the exaggerated systolic and PP responses to ANG II and the higher MBP level after hydralazine most likely reflect a structural modification of the arterial wall such as hypertrophic remodelling in F344.

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“…As such, sodium retention may not be evident. Indeed, most studies of the early phase of hypertension (especially in individuals less than 35 years old) have reported that total exchangeable sodium and plasma volume tend to be low (117)(118)(119)(120) and plasma renin and cathecholamine levels are often elevated (30). Furthermore, the early hypertension mediated by uric acid has been shown to be greatest under the setting of a low-salt diet (60), which may reflect the fact that a low-salt diet enhances activation of the renin angiotensin system.…”

Section: Overview Of the Pathway For Development Of Hypertensionmentioning

confidence: 99%

A Single Pathway for the Development of Essential Hypertension

Kanellis

Nakagawa

Herrera-Acosta

et al. 2003

Cardiology in Review

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Abnormal relation of extracellular fluid volume and exchangeable sodium with systemic arterial pressure in early borderline essential hypertension

Cited by 10 publications

References 21 publications

A linear relationship between the ex-vivo sodium mediated expression of two sodium regulatory pathways as a surrogate marker of salt sensitivity of blood pressure in exfoliated human renal proximal tubule cells: The virtual renal biopsy

A linear relationship between the ex-vivo sodium mediated expression of two sodium regulatory pathways as a surrogate marker of salt sensitivity of blood pressure in exfoliated human renal proximal tubule cells: The virtual renal biopsy

Different vascular responsiveness to angiotensin II in two normotensive rat strains

A Single Pathway for the Development of Essential Hypertension

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