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The breakthrough of the secrets of hypertension and the renin-angiotensin-aldosterone system (RAAS) is one of the legends of medicine. The first chapter is the one of Tigerstedt's experiments about renin, and Loesch and Gollblatt's model of renal hypertension. The race to elucidate the mechanisms of angiotensin, angiotensinogen and the angiotensin conversion enzyme cascade, by Braun Menéndez and Page teams, is a second chapter. The puzzle of this elegant cascade is completed by aldosterone isolation by the collaboration of Tait spouses and Tadeus Rechstein. As a corollary of these findings, Conn made the first description of primary hyperaldosteronism. The elucidation of RAAS pathophysiology naturally led to the synthesis of the antihypertensive captopril by Ondetti and Cushman, thereby opening the modern era of ACE inhibitors and ARII blockers. In March 2020, a viral pandemic caused by SARS-Cov-2 ignites the entire planet. This new coronavirus uses the RAAS angiotensin conversion enzyme type 2 (ACE-2) as a gateway. The SARS-CoV-2/ACE-2 signalling pathway and its pathological effects on the cardio-respiratory and renal system of these patients initiate a new chapter. The interaction of SARS-Cov-2/ACE-2 axis with anti-hypertensive agents, as well as with ACE-2 activators and ACE-2 homologs, takes a part of an active international study searching for therapeutic targets. This modern research, summarized in this article, will further develop our knowledge of RAAS and, hopefully, will improve the management of COVID-19 patients.

In recent years, a greater interest has been focused on primary aldosteronism (PA), which shows a higher prevalence rate than previously thought. The consequences of PA are life threatening such as a refractory hypertension with serious cardiovascular damages.The evaluation of a suspected PA should follow a step-by-step approach (screening test, then confirmatory test and, in some cases, adrenal venous sampling). This protocol may seem tedious, but it allows an accurate etiologic diagnosis that leads to an appropriate therapy with better blood pressure control,improvement of quality of life, and, in some cases even,cure of hypertension.

Almost one third of men and women smoke in Belgium. Besides the well known tobacco's neck and cardiopulmonary systems adverse effects as well as associated neoplasms, today we recognize other deleterious consequences of tobacco on the neuroendocrine, thyroid and reproductive systems. Not only active smokers but also the fetus carried by a smoking mother is at risk for important health problems. Tobacco is a recognized risk factor of occurrence of ophtalmopathy. Some of the active components of tobacco as the thiocyanates are goitrogenic. Tobacco is a risk factor for men and women's infertility. Newborns from parents that smoke are at risk for sudden death. These consequences represent a major public health issue. A campaign for smoking cessation has been recently launched by the Federation of Public Health Service and the INAMI in Belgium.

Brain injuries namely traumatic brain injuries (TBI) and subarachnoid haemorrhage (SAH) are relevant causes of acquired adult hypopituitarism, perhaps more prevalent than ever believed. TBI represent a major health problem with an annual incidence of 300 cases per 100.000. SAH affects six new cases per 1.000.000 habitants in USA. In Belgium we estimate nearly 30.000 new TBI cases and 600 SAH cases per year. In the English literature, TBI secondary hypopituitarism has been well documented in 14 retrospective and prospective series accounting for 1.077 cases. In all these series the main pituitary deficits were: GH (14%), ACTH (14%), gonadotrope (18%), TSH (7%) and diabetes insipidus (4%). SAH was documented as a cause of hypopituitarism in three retrospective series accounting for 110 cases and in one prospective series. In all these series main pituitary deficits were GH (25%), ACTH (15%), gonadotrope (8.5%), TSH (6%) and diabetes insipidus (4%). In this review, we analyze recent data and discuss diagnostic and treatment features of secondary hypopituitarism due TBI and SAH.