Effect of glucocorticoids on renal dopamine production

Aguirre, J.; Ibarra, Fernando; Barontini, Marta; Arrizurieta, Elvira; Armando, Inés

doi:10.1016/s0014-2999(99)00121-1

Cited by 19 publications

(15 citation statements)

References 23 publications

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“…Acute administration of glucocorticoids produces diuresis and natriuresis, an effect more clearly demonstrable during the first 12 hours of administration, while chronic administration of the glucocorticoid attenuates renal water and sodium excretion [11], [12]. Our findings provided a clear answer for this phenomenon.…”

Section: Discussionmentioning

confidence: 51%

“…It is postulated that acute glucocorticoid administration produces potent diuresis and natriuresis, possibly acting in the natriuretic peptide system in the kidney [6], [7], [8], [9], [10]. However, it cannot account for the fact that chronic glucocorticoid administration attenuates renal water and sodium excretion in intact rats [11], [12]. The precise mechanism underlying these paradoxical finding is unclear.…”

Section: Introductionmentioning

confidence: 99%

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Inhibition of Dehydration-Induced Water Intake by Glucocorticoids Is Associated with Activation of Hypothalamic Natriuretic Peptide Receptor-A in Rat

et al. 2010

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Atrial natriuretic peptide (ANP) provides a potent defense mechanism against volume overload in mammals. Its primary receptor, natriuretic peptide receptor-A (NPR-A), is localized mostly in the kidney, but also is found in hypothalamic areas involved in body fluid volume regulation. Acute glucocorticoid administration produces potent diuresis and natriuresis, possibly by acting in the renal natriuretic peptide system. However, chronic glucocorticoid administration attenuates renal water and sodium excretion. The precise mechanism underlying this paradoxical phenomenon is unclear. We assume that chronic glucocorticoid administration may activate natriuretic peptide system in hypothalamus, and cause volume depletion by inhibiting dehydration-induced water intake. Volume depletion, in turn, compromises renal water excretion. To test this postulation, we determined the effect of dexamethasone on dehydration-induced water intake and assessed the expression of NPR-A in the hypothalamus. The rats were deprived of water for 24 hours to have dehydrated status. Prior to free access to water, the water-deprived rats were pretreated with dexamethasone or vehicle. Urinary volume and water intake were monitored. We found that dexamethasone pretreatment not only produced potent diuresis, but dramatically inhibited the dehydration-induced water intake. Western blotting analysis showed the expression of NPR-A in the hypothalamus was dramatically upregulated by dexamethasone. Consequently, cyclic guanosine monophosphate (the second messenger for the ANP) content in the hypothalamus was remarkably increased. The inhibitory effect of dexamethasone on water intake presented in a time- and dose-dependent manner, which emerged at least after 18-hour dexamethasone pretreatment. This effect was glucocorticoid receptor (GR) mediated and was abolished by GR antagonist RU486. These results indicated a possible physiologic role for glucocorticoids in the hypothalamic control of water intake and revealed that the glucocorticoids can act centrally, as well as peripherally, to assist in the normalization of extracellular fluid volume.

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Section: Discussionmentioning

confidence: 51%

Section: Introductionmentioning

confidence: 99%

Inhibition of Dehydration-Induced Water Intake by Glucocorticoids Is Associated with Activation of Hypothalamic Natriuretic Peptide Receptor-A in Rat

et al. 2010

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“…Previous evidence showed that glucocorticoids increased blood pressure and increased GFR. Their effects are also time-dependent, which begin to appear after 1-day Dex treatment (Handa et al, 1984;Aguirre et al, 1999). Our study did show that there was a trend that Dex may slightly raise blood pressure and GFR, but there were no statistically significant differences between Dex-treated rats and vehicle-treated rats because of the short treatment period and small sample size (Supplemental Data).…”

Section: Glucocorticoids Increase Renal Npr-a Expressionmentioning

confidence: 60%

Glucocorticoids Improve Renal Responsiveness to Atrial Natriuretic Peptide by Up-Regulating Natriuretic Peptide Receptor-A Expression in the Renal Inner Medullary Collecting Duct in Decompensated Heart Failure

Liu

Chen²,

Kang³

et al. 2011

J Pharmacol Exp Ther

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In heart failure, the renal responsiveness to exogenous and endogenous atrial natriuretic peptide (ANP) is blunted. The mechanisms of renal hyporesponsiveness to ANP are complex, but one potential mechanism is decreased expression of natriuretic peptide receptor-A (NPR-A) in inner medullary collecting duct (IMCD) cells. Newly emerging evidence shows that glucocorticoids could produce potent diuresis and natriuresis in patients with heart failure, but the precise mechanism is unclear. In the present study, we found dexamethasone (Dex) dramatically increased the expression of NPR-A in IMCD cells in vitro. The NPR-A overexpression induced by Dex presented in a time-and dose-dependent manner, which emerged after 12 h and peaked after 48 h. The cultured IMCD cells were then stimulated with exogenous rat ANP. Consistent with the findings with NPR-A expression, Dex greatly increased cGMP (the second messenger for the ANP) generation in IMCD cells, which presented in a time-and dose-dependent manner as well. In rats with decompensated heart failure, Dex dramatically increased NPR-A expression in inner renal medulla, which was accompanied by a remarkable increase in renal cGMP generation, urine flow rate, and renal sodium excretion. It is noteworthy that Dex dramatically lowered plasma ANP, cGMP levels, and left ventricular end diastolic pressure. These favorable effects induced by Dex were glucocorticoid receptor (GR)-mediated and abolished by the GR antagonist 17␤-hydroxy-11␤-[4-dimethylamino phenyl]-17␣-[1-propynyl]estra-4,9-dien-3-one (RU486). Collectively, glucocorticoids could improve renal responsiveness to ANP by up-regulating NPR-A expression in the IMCD and induce a potent diuretic action in rats with decompensated heart failure.

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“…2) Prednisone, a glucocorticoid that has renal specific vasodilator properties, can increase renal plasma flow and glomerular filtration rate (GFR) with no changes in glomerular filtration fraction. [3][4][5] In addition, glucocorticoids may have important regulatory effects on natriuretic peptides and their receptors. In previous studies, we found that prednisone had potent diuretic effects in patients with stable congestive heart failure, and could restore renal function and elicit potent diuretic effects even in heart failure patients with refractory diuretic resistance.…”

mentioning

confidence: 99%

Prednisone Adding to Usual Care Treatment for Refractory Decompensated Congestive Heart Failure

Zhang

Liu

et al. 2008

Int. Heart J.

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SUMMARYThe aim of the present study was to determine if prednisone, a glucocorticoid, added to conventional treatment for patients with decompensated congestive heart failure (DCHF) refractory to the conventional care, results in significant relief of congestive symptoms and improvement of clinical status.Diuretic-based strategies, as the mainstay in DCHF management, are not always effective in eliciting diuresis. However, the addition of prednisone to standard care may induce potent diuresis in this clinical setting.Thirty-five patients with DCHF were enrolled in the study, and prednisone (1 mg/kg/ day with maximum dosage of 60 mg/day) was added to the standard treatment. Primary endpoints were the effects on daily urine volume, patient and physician assessed dyspnea and global clinical status, and changes in renal function.The addition of prednisone induced potent diuresis with time. As a result of the diuresis, congestive symptoms improved markedly in 80% and global clinical status improved markedly in 68.6% of the DCHF patients at the end of the study (P < 0.001). The change in serum creatinine from baseline was -12.21 µmol/L (P < 0.05).Adding prednisone to conventional care in the patients with refractory DCHF induced potent diuresis accompanied by a dramatic relief of congestive symptoms and improvements in clinical status and renal function. (Int Heart J 2008; 49: 587-595)

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Effect of glucocorticoids on renal dopamine production

Cited by 19 publications

References 23 publications

Inhibition of Dehydration-Induced Water Intake by Glucocorticoids Is Associated with Activation of Hypothalamic Natriuretic Peptide Receptor-A in Rat

Inhibition of Dehydration-Induced Water Intake by Glucocorticoids Is Associated with Activation of Hypothalamic Natriuretic Peptide Receptor-A in Rat

Glucocorticoids Improve Renal Responsiveness to Atrial Natriuretic Peptide by Up-Regulating Natriuretic Peptide Receptor-A Expression in the Renal Inner Medullary Collecting Duct in Decompensated Heart Failure

Prednisone Adding to Usual Care Treatment for Refractory Decompensated Congestive Heart Failure

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