title: Partial deficiency of adrenal 11-hydroxylase. A possible cause of primary hypertension.
abstract: Results of supraphysiological adrenocorticotropic hormone (ACTH) stimulation of biosynthetic pathways of adrenal zona fasciculata indicate that a deficiency of 11-hydroxylase exists in patients with essential hypertension. The deficiency is suggested by the much greater stimulus of synthesis of deoxycorticosterone (DOC) and deoxycortisol in hypertensive subjects than in controls (p less than 0.001). No significant difference in the synthesis of cortisol, corticosterone, progesterone, 17-hydroxyprogesterone (17-OHP), and delta-4-androstenedione (D4) was observed between the two groups. The ratios for synthesis of DOC and corticosterone and for deoxycortisol and cortisol found in hypertensive patients were significantly higher than those found in controls (p less than 0.001); no significant difference was observed in the synthesis of 17-OHP and progesterone. The synthesis of DOC and deoxycortisol was not significantly correlated with either blood pressure or plasma renin activity. Plasma renin activity was significantly lower in hypertensive subjects than in normotensive subjects (p less than 0.0001), while no difference was found in aldosterone secretion between the two groups. The 11-hydroxylase deficiency in the adrenal zona fasciculata may be one of the genetic factors causing hypertension together with environmental factors (particularly salt intake and work-related stress). The investigation performed in our study may be useful for the evaluation of adrenal zona fasciculata enzymatic activities during the study of hypertensive patients.
authors.forename: G
authors.initials: G
authors.lastname: de Simone
authors.forename: A P
authors.initials: AP
authors.lastname: Tommaselli
authors.forename: R
authors.initials: R
authors.lastname: Rossi
authors.forename: R
authors.initials: R
authors.lastname: Valentino
authors.forename: R
authors.initials: R
authors.lastname: Lauria
authors.forename: F
authors.initials: F
authors.lastname: Scopacasa
authors.forename: G
authors.initials: G
authors.lastname: Lombardi
mesh_terms: D015065:17-Hydroxycorticosteroids / Q000097:blood*; D019326:17-alpha-Hydroxyprogesterone; D000312:Adrenal Hyperplasia, Congenital; D000324:Adrenocorticotropic Hormone / Q000494:pharmacology; D000328:Adult; D000450:Aldosterone / Q000097:blood; D003350:Cortodoxone / Q000097:blood*; D003900:Desoxycorticosterone / Q000097:blood; D005260:Female; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D006908:Hydroxyprogesterones / Q000097:blood; D006973:Hypertension / Q000097:blood / Q000201:enzymology* / Q000209:etiology; D008297:Male; D008875:Middle Aged; D012083:Renin / Q000097:blood; D013250:Steroid Hydroxylases / Q000172:deficiency*
chemical_list: D015065:17-Hydroxycorticosteroids; D006908:Hydroxyprogesterones; D003900:Desoxycorticosterone; D000450:Aldosterone; D019326:17-alpha-Hydroxyprogesterone; D000324:Adrenocorticotropic Hormone; D013250:Steroid Hydroxylases; D012083:Renin; D003350:Cortodoxone; D006854:Hydrocortisone