Regulation of renal hemodynamics after protein feeding: effects of proximal and distal diuretics

Woods, L. L.; Smith, Brendan E.; Db, Young

doi:10.1152/ajpregu.1993.264.2.r337

Cited by 9 publications

(10 citation statements)

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“…24–26 Thus, this mechanism might account for the renal vasodilation after feeding the mixed meal in the present study. Regardless of the mechanisms that mediate postprandial increases in GFR and RBF, it is clear from the present study that this vasodilation and the normal circadian fluctuation in RBF was not disturbed by baroreflex activation, despite reductions in the chronic set point for control of renal hemodynamics.…”

Section: Discussionmentioning

confidence: 57%

Renal Responses to Chronic Suppression of Central Sympathetic Outflow

et al. 2012

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Chronic electrical activation of the carotid baroreflex produces sustained reductions in sympathetic activity and arterial pressure and is currently being evaluated as hypertension therapy for patients with resistant hypertension. However, the chronic changes in renal function associated with natural suppression of sympathetic activity are largely unknown. In normotensive dogs we investigated the integrative cardiovascular effects of chronic baroreflex activation (2 weeks) alone and in combination with the calcium channel blocker amlodipine, which is commonly used in the treatment of resistant hypertension. During baroreflex activation alone, there were sustained decreases in mean arterial pressure (17 ± 1 mm Hg) and plasma [norepinephrine] (NE, ~35%), with no change in plasma renin activity (PRA). Despite low pressure, sodium balance was achieved due to decreased tubular reabsorption, because GFR and renal blood flow decreased 10–20%. After 2 weeks of amlodipine, arterial pressure was also reduced 17 mm Hg, but with substantial increases in NE and PRA, and no change in GFR. In the presence of amlodipine, baroreflex activation greatly attenuated neurohormonal activation and pressure decreased even further (by 11 ± 2 mm Hg). Moreover, during amlodipine administration the fall in GFR with baroreflex activation was abolished. These findings suggest that the chronic blood pressure lowering effects of baroreflex activation are due, at least in part, to sustained inhibition of renal sympathetic nerve activity and attendant decreases in sodium reabsorption prior to the macula densa. Tubuloglomerular feedback constriction of the afferent arterioles may account for reduced GFR, a response abolished by amlodipine, which dilates the preglomerular vasculature.

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Section: Discussionmentioning

confidence: 57%

Renal Responses to Chronic Suppression of Central Sympathetic Outflow

et al. 2012

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“…Either acute or chronic protein load increases GFR (1,8,21,22,29,31,33,36,37). To investigate whether COX-2 expression in kidney cortex correlates with GFR variations in response to alterations in protein intake, GFR was measured in rats on the different protein diets (26).…”

Section: Resultsmentioning

confidence: 99%

“…Alteration of luminal NaCl delivery to the MD is the signal for MD regulation of TGF and renin release, with increased salt delivery stimulating TGF and decreased salt delivery stimulating renin release (2,12,32,35). High-protein intake has been reported to cause a selective hypertrophy of the thick ascending limb and increased NaCl reabsorption in this segment and/or in the proximal tubule, leading to reduced NaCl delivery to the MD (1,31,32,36,37). COX-2 expression in the MD/cTALH increases in conditions associated with reduced NaCl delivery to the MD (18 -20, 32, 34, 41).…”

mentioning

confidence: 99%

Role of renal cortical cyclooxygenase-2 expression in hyperfiltration in rats with high-protein intake

Yao

Xu²,

Qi³

et al. 2006

American Journal of Physiology-Renal Physiology

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Renal cortical cyclooxygenase-2 (COX-2) is restricted to the macula densa and adjacent cortical thick ascending limbs (MD/cTALH). Renal cortical COX-2 increases in response to diabetes and renal ablation, both of which are characterized by hyperfiltration and reduced NaCl delivery to the MD due to increased proximal NaCl reabsorption. High-protein intake also induces hyperfiltration and decreases NaCl delivery to the MD due to increased NaCl reabsorption proximally. We investigated whether high protein induces cortical COX-2 and whether cortical COX-2 contributes to high protein-induced hyperfiltration and increased intrarenal renin biosynthesis. Cortical COX-2 increased after protein loading but decreased after protein restriction. COX-2 inhibition attenuated high protein-induced hyperfiltration but had no effect on high protein-induced intrarenal renin elevation. Therefore, induction of cortical COX-2 contributed to high protein-induced hyperfiltration but not intrarenal renin elevation. In the kidney cortex, neuronal nitric oxide synthase (nNOS) is also localized to the MD, and interactions between intrarenal nNOS and COX-2 systems have been proposed. Cortical COX-2 elevation seen in salt restriction was blocked by nNOS inhibiton. Cortical nNOS expression also increased after protein loading, and inhibition of nNOS activity completely reversed high protein-induced cortical COX-2 elevation and hyperfiltration. These results indicate that NO is a mediator of high protein-induced cortical COX-2 elevation and suggest that both intrarenal nNOS and COX-2 systems appear to regulate afferent arteriolar tone and subsequent hyperfiltration seen in high-protein intake.

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“…The ingestion of a protein‐rich meal or the intravenous infusion of amino acids leads to a 25–60% increase in the glomerular filtration rate (GFR) and renal plasma flow (RPF) in animals and humans 1–3 This temporary increase in GFR and RPF reflects the ability of the kidney to enhance its function when an appropriate stimulus is applied, indicating the magnitude of the renal reserve.…”

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confidence: 99%

Renal response to an acute protein challenge in pregnant women with borderline hypertension

et al. 2007

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Mid-term borderline HP failed to increase CCr as much as NP did after a protein challenge, suggesting altered functional response of the nephron or lessened sensitivity of renal vasculature to additional vasodilator stimuli. These results support the interest of additional prospective studies with a larger number of patients to confirm these findings and evaluate the value of RR tests as predictors of outcome of pregnancies at risk.

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Regulation of renal hemodynamics after protein feeding: effects of proximal and distal diuretics

Cited by 9 publications

References 0 publications

Renal Responses to Chronic Suppression of Central Sympathetic Outflow

Renal Responses to Chronic Suppression of Central Sympathetic Outflow

Role of renal cortical cyclooxygenase-2 expression in hyperfiltration in rats with high-protein intake

Renal response to an acute protein challenge in pregnant women with borderline hypertension

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