Furosemide Treatment, Angiotensin II, and Renal Growth and Development in the Rat

Lane, Pascale H.

doi:10.1203/00006450-199506000-00013

Cited by 11 publications

(12 citation statements)

References 43 publications

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“…These results are in line with the previous finding that furosemide treatment increases V G in normal rats (32). Glomerular hypertrophy has been pointed out as one of the initiating factors leading to the development of glomerulosclerosis (23,29), along with an elevation of P GC (5,17,18,31), presumably because these two abnormalities synergistically increase mechanical stretching of the glomerular wall (13), thus leading to glomerular cell proliferation and to the production of inflammatory mediators (21).…”

Section: Discussionsupporting

confidence: 91%

An association of losartan-hydrochlorothiazide, but not losartan-furosemide, completely arrests progressive injury in the remnant kidney

Arias

Souza

Malheiros

et al. 2016

American Journal of Physiology-Renal Physiology

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We have previously shown that an association of losartan and hydrochlorothiazide, initiated 1 mo after 5/6 nephrectomy (Nx), reversed hypertension and albuminuria and promoted lasting renoprotection. In this new study, we investigated whether equal or even better protection could be obtained by combining losartan and furosemide. Nx was performed in 58 Munich-Wistar rats. One month later, tail-cuff pressure and albuminuria were markedly elevated. At this time, Nx rats were distributed among the following four groups: untreated Nx rats, Nx rats that received losartan, Nx rats that received losartan + hydrochlorothiazide, and Nx rats that received losartan + furosemide. Seven months later, Nx rats exhibited high mortality, severe hypertension, albuminuria, glomerulosclerosis, and interstitial fibrosis. Losartan treatment limited mortality and attenuated the renal and hemodynamic abnormalities associated with Nx. As previously shown, the losartan + hydrochlorothiazide association normalized tail-cuff pressure and albumin, prevented renal injury, and reduced mortality to zero. The losartan + furosemide treatment failed to reduce tail-cuff pressure or albumin to normal and prevented renal injury less efficiently than the losartan and hydrochlorothiazide regimen. The reasons for the differing efficacies of the losartan + furosemide and losartan + hydrochlorothiazide schemes are unclear and may include beneficial nondiuretic actions of thiazides, such as vasorelaxation and antiproliferative activity. These results refute the established concept that thiazides and thiazide-like diuretics are ineffective at advanced chronic kidney disease stages. Rather, they suggest that, in view of their renoprotective action, these compounds may even be preferable to loop diuretics in the management of hypertension in advanced chronic kidney disease.

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Section: Discussionsupporting

confidence: 91%

An association of losartan-hydrochlorothiazide, but not losartan-furosemide, completely arrests progressive injury in the remnant kidney

Arias

Souza

Malheiros

et al. 2016

American Journal of Physiology-Renal Physiology

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“…This model produces reliable and severe NC in a significant proportion of rats (50% – 100%) (Table 1). Previous studies have shown that weanling rats provide a clinically relevant model system to study how chronic changes in dietary sodium and chloride depletion modulate the ECF fluid volume, total body growth, muscle protein synthesis, and the activation of the systemic and local renin-angiotensin system (21–24). The rapidly growing organism of preterm infants and young rats, needs electrolytes to support the expansion of ECF volume required for normal grow (21, 25–27).…”

Section: Discussionmentioning

confidence: 99%

Development of an animal model of nephrocalcinosis via selective dietary sodium and chloride depletion

et al. 2012

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Background Nephrocalcinosis (NC) is an important clinical problem seen in critically ill pre-term neonates treated with loop diuretics. No reliable animal models are available to study the pathogenesis of NC in preterm infants. The purpose of this study was to develop a reproducible and clinically relevant animal model of NC for these patients, and to explore the impact of extracellular fluid (ECF) volume contraction induced by sodium and chloride depletion in this process. Methods Three-week old weanling Sprague-Dawley rats were fed diets deficient in either chloride or sodium and chloride. A sub-group of rats from each dietary group was injected daily with furosemide (40 mg/kg; i.p.). Results Rats fed a control diet, with or without furosemide, or a chloride depleted diet alone, did not develop NC. In contrast, 50% of the rats injected with furosemide and fed the chloride depleted diet developed NC. Moreover, 94% of the rats fed the combined sodium/chloride depleted diet developed NC, independently of furosemide use. NC was associated with the development of severe ECF volume contraction, hypochloremic, hypokalemic metabolic alkalosis, increased phosphaturia, and growth retardation. Conclusion Severe ECF volume contraction induced by chronic sodium and chloride depletion appears to play an important role in the pathogenesis of NC.

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“…Chronic use of the diuretic furosemide, which blocks the NKCC2 co-transporter, results in the induction of COX-2 (28) and the stimulation of renin secretion (29) and causes a clinical phenotype similar to HPS/aBS: Salt and water loss, hyposthenuria, nephrocalcinosis, and poor growth (30,31). To elucidate further the pathogenetic role of PGE 2 in HPS/aBS, we studied EP receptor function in mice deficient for a distinct subtype of the EP receptor after chronic treatment with furosemide.…”

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confidence: 99%

Dominant Role of Prostaglandin E2 EP4 Receptor in Furosemide-Induced Salt-Losing Tubulopathy

Nüsing

Treude

Weißenberger

et al. 2005

Journal of the American Society of Nephrology

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Increased formation of prostaglandin E 2 (PGE 2 ) is a key part of hyperprostaglandin E syndrome/antenatal Bartter syndrome (HPS/aBS), a renal disease characterized by NaCl wasting, water loss, and hyperreninism. Inhibition of PGE 2 formation by cyclo-oxygenase inhibitors significantly lowers patient mortality and morbidity. However, the pathogenic role of PGE 2 in HPS/aBS awaits clarification. Chronic blockade of the Na-K-2Cl co-transporter NKCC2 by diuretics causes symptoms similar to HPS/aBS and provides a useful animal model. In wild-type (WT) mice and in mice lacking distinct PGE 2 receptors (EP1 In summary, these findings demonstrate that the EP4 receptor mediates PGE 2 -induced renin secretion and that EP1, EP3, and EP4 receptors all contribute to enhanced PGE 2 -mediated salt and water excretion in the HPS/aBS model.

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Furosemide Treatment, Angiotensin II, and Renal Growth and Development in the Rat

Cited by 11 publications

References 43 publications

An association of losartan-hydrochlorothiazide, but not losartan-furosemide, completely arrests progressive injury in the remnant kidney

An association of losartan-hydrochlorothiazide, but not losartan-furosemide, completely arrests progressive injury in the remnant kidney

Development of an animal model of nephrocalcinosis via selective dietary sodium and chloride depletion

Dominant Role of Prostaglandin E2 EP4 Receptor in Furosemide-Induced Salt-Losing Tubulopathy

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