Browsing by Author "Carvajal M C."

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    11β-hydroxysteroid dehydrogenase activity in patients with hypertension and low plasma renin activityActividad de 11 beta hidroxiesteroide dehidrogenasa tipo 2 en hipertensos chilenos
    (2002) Fardella B C.; Mosso G L.; Carvajal M C.; Campino J C.; Rojas O A.; González P A.; Barraza M A.; Montero L J.; NCD Risk Factor Collaboration (NCD-RisC)
    Background: Half of hypertensive patients with low plasma renin activity have a primary hyperaldosteronism. Among the remaining half, 11β-hydroxysteroid dehydrogenase type 2 (11βHSD2) deficiency plays an important role. This enzyme catalyzes the conversion of cortisol to cortisone, avoiding the interaction of cortisol with the mineralocorticoid receptor. If the enzyme fails, cortisol will stimulate sodium and water reabsorption and increase blood pressure. Aim: To determine biochemical alterations, suggestive of 11βHSD2 deficiency, in low-renin hypertensive patients. Patients and Methods: Twenty eight hypertensive patients with a plasma renin activity of less than 0.5 ng/ml/h and with a plasma aldosterone of less than 5 ng/dl were studied. Twenty eight normotensive patients were studied as controls. Serum cortisol (RIA), cortisone (ELISA) and the serum cortisol/cortisone ratio were determined in all of them, between 9 and 10 AM. Measurements were confirmed by high pressure liquid chromatography. The serum cortisol/cortisone ratio was considered abnormal when its Ln (cortisol/cortisone) value was over 2 standard deviations of the mean. Results: Serum cortisol was higher in hypertensive subjects than in controls (11.1±3.3 and 9.2±2.8 μg/dl, respectively; p <0.05). No differences were observed in serum cortisone (3.4±1.3 and 3.7±1.2 μg/dl, respectively). Four hypertensive subjects had an abnormally high Ln (cortisol/cortisone) value (1.86; 1.73; 2.07 and 2.01, considering a normal value of less than 1.61). Conclusions: Four of 28 hypertensive subjects with low plasma renin activity and aldosterone had biochemical alterations suggestive of 11βHSD2 deficiency (Rev Méd Chile 2002; 130: 1201-8).
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    Free urinary cortisol is elevated in patients with low-renin essential hypertensionElevación del cortisol urinario en hipertensos esenciales hiporreninémicos
    (2004) Mosso G L.; Fardella B C.; Krall O P.; Carvajal M C.; Rojas O A.; Fardella B C.; NCD Risk Factor Collaboration (NCD-RisC)
    Background: Glucocorticoids play a key role in blood pressure (BP) control and are associated with hypertension in patients with Cushing's syndrome. A number of reports indicate that cortisol (F) may be involved in etiology of essential hypertension (EH). F can bind to the mineralocorticoid receptor, triggering both sodium and water reabsorption in kidney, increase BP and cause renin suppression. Aim: To evaluate urinary free cortisol (UFF) excretion as a potential intermediate phenotype of essential hypertension and correlate F level with plasma renin activity (PRA) and serum aldosterone (SA). Patients and Methods: We recruited 132 EH patients and 16 normotensive healthy controls. Blood samples and 24 hours urine were collected for PRA, SA and UFF analysis. Differences in UFF excretion between sexes were normalized by urinary creatinine (Creat) excretion. The upper limit of UFF/Creat was determined in normotensives considering the mean value plus 2 standard deviations. According to this value, subjects were classified as having high or normal UFF. Results: In EH patients and in normotensives, the UFF/Creat was 36.9±17.0 μg/gr and 30.9±8.8 μg/gr, respectively. The upper limit was set at 48.5 μg/gr. A high UFF/Creat was found in 20/132 EH (15%) patients and 0/16 normotensive subjects. EH patients with high UFF showed lower PRA levels than patients with normal cortisol levels (0.78±0.47 vs. 1.13±0.66 ng/ml*h, respectively, p=0.027) and lower SA values (4.52±1.65 vs 6.34±3.37 ng/dl, respectively, p=0.018). There was a negative correlation between UFF and PRA (r=-0.176, p=0.044) and between UFF and SA (r=-0.183, p=0.036). Conclusions: We have identified a subgroup of EH patients with increased UFF excretion. Patients with the highest UFF showed lower renin and aldosterone levels. These data suggest a potential influence of cortisol in the genesis of hypertension.