نتایج جستجو برای: aldosterone escape
تعداد نتایج: 41626 فیلتر نتایج به سال:
Accumulating evidence indicates that aldosterone plays a critical role in the mediation of oxidative stress and vascular damage. NADPH oxidase has been recognized as a major source of oxidative stress in vasculature. However, the relation between NADPH oxidase in aldosterone-mediated oxidative stress in endothelial cells remains to be ascertained. The present study aimed to investigate the rel...
There are many reports for involvement of ATP-sensitive potassium channels in pancreatic, cardiac and vascular smooth muscle cells. This study examined the effect of single doses of K+ channel openers diazoxide, minoxidil and K+ channel blockers chlorpropamide, glibenclamide on serum concentration of aldosterone in male rats. Blood samples were obtained 60 minutes after drug treatment and serum...
Accumulating evidence indicates that aldosterone plays a critical role in the mediation of oxidative stress and vascular damage. NADPH oxidase has been recognized as a major source of oxidative stress in vasculature. However, the relation between NADPH oxidase in aldosterone-mediated oxidative stress in endothelial cells remains to be ascertained. The present study aimed to investigate the rel...
Mineralocorticoid receptor antagonists for the treatment of hypertension and the metabolic syndrome.
I ncreasing evidence suggests a link between the metabolic syndrome and aldosterone. Patients with obesity and the metabolic syndrome have been found to have increased adrenal production of aldosterone and increased cortisol levels , whereas weight reduction is associated with a decrease in aldosterone. 6 A high-fat diet has been shown to lead to an upregulation of mineralocorticoid expression,...
Prostasin has been demonstrated to be an activator of epithelial sodium channels in cultured renal and bronchial epithelial cells. In this study, we evaluated the effects of adenovirus-mediated gene transfer of human prostasin on blood pressure regulation and sodium reabsorption in Wistar rats. Expression of human prostasin mRNA was identified in rat adrenal gland, liver, kidney, heart, lung, a...
BACKGROUND The renal damage that is present in primary aldosteronism might reflect functional and potentially reversible abnormalities that are initiated by glomerular hyperfiltration. The aim of this study was to investigate the relationships of plasma renin and aldosterone concentrations with renal outcomes after treatment of primary aldosteronism. DESIGN, SETTING, PARTICIPANTS, AND MEASURE...
Background: Aldosterone has been assumed to be implicated in left ventricular hypertrophy (LVH). Preventing the progression of LVH in the early period of end-stage renal disease (ESRD) can increase patient survival. In this study, therefore, we analyzed the relationship between aldosterone level and LVH in ESRD patients who underwent hemodialysis at Fatemeh Zahra Hospital and Imam Khomeini Hosp...
Long term administration of aldosterone (1) or desoxycorticosterone acetate (DCA) (2) to normal subjects has been shown, in certain instances, to produce continued renal potassium loss but only transient sodium and chloride retention. This adjustment of the renal response to sodium-retaining adrenal steroids has been termed an "escape" (3) from the expected effects of these compounds, and is se...
Aldosterone increases blood pressure (BP) by stimulating sodium (Na) reabsorption within the distal nephron and collecting duct (CD). Aldosterone also stimulates endothelin-1 (ET-1) production that acts within the CD to inhibit Na reabsorption via a negative feedback mechanism. We tested the hypothesis that this renal aldosterone-endothelin feedback system regulates electrolyte balance and BP b...
1. The present study investigates the role of mineralocorticoids in the pathogenesis of salt retention and ascites in dogs with chronic ligation of the common bile duct (CBDL). 2. After CBDL the natriuretic response to an intravenous sodium load [0.9% sodium chloride solution (150 mmol/l): saline; 10% of body weight] was markedly depressed. Urinary sodium excretion was 285 +/- 62 vs 960 +/- 58 ...
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