[312-POS]: Mechanisms of renal potassium retention during late pregnancy.
Gainesville, United States. In Pregnancy Hypertens, Jan 2015
METHODS: We measured the mRNA expression of WNK1, WNK4, ROMK, H+/K+ - ATPase type 1 (HKA1), H+/K+ - ATPase type 2 (HKA2), and H+ - ATPase in the renal cortex, outer medulla, and inner medulla of virgin (V, n=6), mid pregnant (MP, n=6), and late pregnant (LP, n=6) rats using quantitative real-time PCR.
Renal mechanisms of salt-sensitive hypertension: contribution of two steroid receptor-associated pathways.
Tokyo, Japan. In Am J Physiol Renal Physiol, Jan 2015
Recent studies revealed the involvement of two important signaling pathways in renal tubules that play key roles in electrolyte balance and the maintenance of normal blood pressure: the β2 adrenergic stimulant-GR-WNK4-NCC pathway, which is active in distal convoluted tubules 1 (DCT1); and the Rac1-MR pathway, which is active in distal convoluted tubules 2 (DCT2), connecting tubules (CNT), and collecting ducts (CD).
Disorders of aldosterone synthesis, secretion, and cellular function.
Saint Petersburg, United States. In Curr Opin Pediatr, Aug 2014
Secondary hypoaldosteronism (pseudohypoaldosteronism) occurs as a consequence of mutations in genes encoding the mineralocorticoid receptor (MR), the three subunits of the aldosterone-responsive, amiloride-sensitive nonvoltage-gated sodium channel encoded by SCNN1A, SCNN1B, and SCNN1G, the gene that regulates posttranslational phosphorylation (encoded by WNK4) of the thiazide-sensitive sodium chloride cotransporter encoded by SLC12A3, and those that regulate phosphorylation and ubiquitination of cofactors encoded by WNK1, KLH3, and CUL3 that affect WNK4 function.
Renal nerves, WNK4, glucocorticoids, and salt transport.
Portland, United States. In Cell Metab, 2011
A study in Nature Medicine (Mu et al., 2011) shows that dietary salt excess, coupled with β-adrenergic stimulation, increases arterial pressure via glucocorticoid receptors and WNK4, suggesting interactions between these systems in the pathogenesis of hypertension.