Research Article Mild Adrenal Steroidogenic Defects and ACTH-Dependent Aldosterone Secretion in High Blood Pressure: Preliminary Evidence João Martin Martins, 1,2 Sónia do Vale, 1,2 and Ana Filipa Martins 1,2 1 Endocrine Department, Hospital Santa Maria and Lisbon Medical School, Professor Egas Moniz Avenue, 1649-028 Lisbon, Portugal 2 Servic ¸o de Endocrinologia, Hospital de Santa Maria, Piso 6, Avenida Professor Egas Moniz, 1649-028 Lisboa, Portugal Correspondence should be addressed to Jo˜ ao Martin Martins; jmartinmartins@sapo.pt Received 13 September 2014; Revised 11 November 2014; Accepted 13 November 2014; Published 15 December 2014 Academic Editor: Andre P. Kengne Copyright © 2014 Jo˜ ao Martin Martins et al. his is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Introduction. Adrenal glands play a major role in the control of blood pressure and mild defects of steroidogenesis and/or inappropriate control of mineralocorticoid production have been reported in high blood pressure (HBP). Patients and Methods. We used a speciic protocol for the evaluation of 100 consecutive patients with inappropriate or recent onset HBP. Speciic methods were used to conirm HBP and to diagnose secondary forms of HBP. In addition we tested adrenal steroidogenesis with the common cosyntropin test, modiied to include the simultaneous measurement of renin and aldosterone besides 17-hydroxyprogesterone (17OHP) and 11-deoxycortisol (S). Results. Secondary forms of HBP were diagnosed in 32 patients, including 14 patients with primary hyperaldosteronism (PA) (14%) and 10 patients with pheochromocytoma (10%). Mild defects of the 21-hydroxylase (21OHD) and 11-hydroxylase (11OHD) enzymes were common (42%). ACTH-dependent aldosterone secretion was found in most patients (54%) and characteristically in those with mild defects of adrenal steroidogenesis (>60%), PA (>75%), and otherwise in patients with apparent essential HBP (EHBP) (32%). Discussion. Mild defects of adrenal steroidogenesis are common in patients with HBP, occurring in almost half of the patients. In those patients as well as in patients with apparent EHBP, aldosterone secretion is commonly dependent on ACTH. 1. Introduction HBP occurs in more than 25% of the adult western population and is a major determinant of mortality, with cardio- and cerebrovascular disease accounting for 30–50% of all deaths [1]. Until recently, HBP was assumed to be idiopathic in over 90% of the cases, and the search for the etiology was a futile clinical exercise in most instances [2]. As an example of changing medical paradigms, secondary forms of HBP, mainly PA, are now considered to account for up to 15% of all cases [3]. Adrenal glands play a major direct role in water and salt balance, mineralocorticoids and glucocorticoids, and in heart output and vascular tone, catecholamines; they are therefore a major determinant of blood pressure levels in normal conditions [3–5]. Speciic adrenal diseases like PA, Cushing’s syndrome, pheochromocytoma, and some cases of congenital adrenal hyperplasia (CAH) and glucocorticoid-remediable aldosteronism (GRA) are well recognized forms of secondary HBP [1–7]; however, except for PA, all are deemed to be very rare. A more general involvement of the adrenals may occur in HBP. Recent research identiies mild defects of the inal steps of glucocorticoid and/or mineralocorticoid synthesis, namely, defects of the 11-hydroxylase enzyme and abnormal control of aldosterone secretion, ACTH-dependent aldos- terone secretion, as common and related phenomena in patients with HBP [8–12]. We tested adrenal steroidogenesis and mineralocorticoid production, using the common cosyn- tropin test, modiied to include the measurement of renin and aldosterone, besides cortisol, 17OHP, and S, in patients Hindawi Publishing Corporation International Journal of Endocrinology Volume 2014, Article ID 295724, 8 pages http://dx.doi.org/10.1155/2014/295724