fludrocortisone-acetate and Hypertension

fludrocortisone-acetate has been researched along with Hypertension* in 2 studies

Other Studies

2 other study(ies) available for fludrocortisone-acetate and Hypertension

Article	Year
Early hypertension and prolonged mineralocorticoid therapy discontinuation in a child with salt-wasting 21-hydroxylase deficiency. Journal of endocrinological investigation, 2011, Volume: 34, Issue:2 Topics: Adrenal Hyperplasia, Congenital; Anti-Inflammatory Agents; Child, Preschool; Fludrocortisone; Humans; Hydrocortisone; Hypertension; Infant, Newborn; Male; Mineralocorticoids	2011
Urinary prostasin: a candidate marker of epithelial sodium channel activation in humans. Hypertension (Dallas, Tex. : 1979), 2005, Volume: 46, Issue:4 Prostasin is a serine peptidase hypothesized to regulate epithelial sodium channel (ENaC) activity in animals or on in vitro cultured cells. We investigated whether urinary prostasin may be a candidate marker of ENaC activation in humans. We studied 10 healthy volunteers and 8 hypertensive patients with raised aldosterone-to-renin ratio before and after spironolactone or saline/Florinef suppression test, respectively. Four healthy subjects were also studied before and after saline. Urinary prostasin was evaluated by SDS-PAGE, 2D maps, and Western blotting. Every sample of normotensive individuals was compared with the corresponding sample of urine collected after spironolactone or saline; every sample of hypertensive patients was compared with the corresponding sample of urine collected after saline or Florinef. Prostasin was detectable in all subjects regardless of gender, dietary sodium intake, and spironolactone treatment. Spironolactone (100 mg) increased urinary Na+/K+ ratio and decreased urinary prostasin in normotensives in whom the renin/aldosterone axis was activated by a low Na+ intake, but it was ineffective in individuals with high Na+ intake. Saline infusion also reduced prostasin in normotensive subjects. In contrast, prostasin paradoxically increased in urine of patients affected by primary aldosteronism after volume expansion. By 2D immunoblotting, several protein isoforms were observed, some of them being overexpressed after inhibition tests in patients with primary aldosteronism. In addition to a "basal" aliquot of prostasin, constitutively released in human urine regardless of sodium balance and aldosterone activation, there exists a second "aldosterone-responsive" aliquot modulated by Na+ intake and potentially suitable as candidate marker of ENaC activation. Topics: Adult; Aged; Aldosterone; Biomarkers; Blotting, Western; Case-Control Studies; Diuretics; Dose-Response Relationship, Drug; Epithelial Sodium Channels; Female; Fludrocortisone; Humans; Hyperaldosteronism; Hypertension; Male; Middle Aged; Potassium; Renin; Serine Endopeptidases; Sodium; Sodium Channels; Sodium Chloride; Sodium, Dietary; Spironolactone	2005

Article

Year

Early hypertension and prolonged mineralocorticoid therapy discontinuation in a child with salt-wasting 21-hydroxylase deficiency.

Journal of endocrinological investigation, 2011, Volume: 34, Issue:2

Topics: Adrenal Hyperplasia, Congenital; Anti-Inflammatory Agents; Child, Preschool; Fludrocortisone; Humans; Hydrocortisone; Hypertension; Infant, Newborn; Male; Mineralocorticoids

2011

Urinary prostasin: a candidate marker of epithelial sodium channel activation in humans.

Hypertension (Dallas, Tex. : 1979), 2005, Volume: 46, Issue:4

Prostasin is a serine peptidase hypothesized to regulate epithelial sodium channel (ENaC) activity in animals or on in vitro cultured cells. We investigated whether urinary prostasin may be a candidate marker of ENaC activation in humans. We studied 10 healthy volunteers and 8 hypertensive patients with raised aldosterone-to-renin ratio before and after spironolactone or saline/Florinef suppression test, respectively. Four healthy subjects were also studied before and after saline. Urinary prostasin was evaluated by SDS-PAGE, 2D maps, and Western blotting. Every sample of normotensive individuals was compared with the corresponding sample of urine collected after spironolactone or saline; every sample of hypertensive patients was compared with the corresponding sample of urine collected after saline or Florinef. Prostasin was detectable in all subjects regardless of gender, dietary sodium intake, and spironolactone treatment. Spironolactone (100 mg) increased urinary Na+/K+ ratio and decreased urinary prostasin in normotensives in whom the renin/aldosterone axis was activated by a low Na+ intake, but it was ineffective in individuals with high Na+ intake. Saline infusion also reduced prostasin in normotensive subjects. In contrast, prostasin paradoxically increased in urine of patients affected by primary aldosteronism after volume expansion. By 2D immunoblotting, several protein isoforms were observed, some of them being overexpressed after inhibition tests in patients with primary aldosteronism. In addition to a "basal" aliquot of prostasin, constitutively released in human urine regardless of sodium balance and aldosterone activation, there exists a second "aldosterone-responsive" aliquot modulated by Na+ intake and potentially suitable as candidate marker of ENaC activation.

Topics: Adult; Aged; Aldosterone; Biomarkers; Blotting, Western; Case-Control Studies; Diuretics; Dose-Response Relationship, Drug; Epithelial Sodium Channels; Female; Fludrocortisone; Humans; Hyperaldosteronism; Hypertension; Male; Middle Aged; Potassium; Renin; Serine Endopeptidases; Sodium; Sodium Channels; Sodium Chloride; Sodium, Dietary; Spironolactone

2005