Atrial natriuretic factor effects on cyclic nucleotides in a human renal cell line.

Cole, Francis E.; Rovigatti, Ugo; Iwata, Takeru; Vaughn, James L.; Fröhlich, Edward D.

doi:10.1161/01.hyp.13.6.799

Cited by 6 publications

(1 citation statement)

References 16 publications

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“…Natriuretic peptides elicit their physiological responses through synthesis of cGMP when binding to their receptors. Therefore, cGMP levels in renal cells serves as a useful biological marker for the renal activity of ANP in vitro (Ballermann et al, 1985;Cole et al, 1989). The ANP stimulation test was performed by the method described previously (Kanda et al, 1989).…”

Section: Methodsmentioning

confidence: 99%

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

The Journal of Pharmacology and Experimental Therapeutics

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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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Section: Methodsmentioning

confidence: 99%