Is the Primary Aetiology of Hypertension Unknown? Novel Views on Previous Assumptions
Andras Sikter1* and Christian Sonne2
1Department of Internal Medicine, Municipal Clinic of Szentendre, Hungary
2Department of Bioscience, Aarhus University, Arctic Research Centre (ARC), Denmark
*Corresponding Author: Andras Sikter, Department of Internal Medicine, Municipal Clinic of Szentendre, Hungary.
Received:June 15, 2021; Published: July 14, 2021
Most details of primary hypertension are known, however, it is still unclear how and why the increased activity of angiotensin II and aldosterone cause developing primary hypertension seen worldwide. Here we hypothesize that primary hypertension is an age-related disease initiated by the acidification of the intracellular milieu. The renin-angiotensin-aldosterone system (RAAS), like many other hormones, work through feedback mechanisms, with aldosterone restoring pH and electrolyte changes produced by respiratory acidosis in targeted cardiovascular and kidney cells. High NaCl intake enhances the effect of aldosterone (salt-sensitive hypertension). By contrast, angiotensin II restores H+ and electrolyte abnormalities caused by metabolic acidosis in the targeted cells (salt-resistant hypertension). Aldosterone and angiotensin II decrease H+ concentration synergistically, but act antagonistically on Cl- to HCO3- concentrations. However, both hormones overcompensate acidosis and increase Na+ retention leading to increased circulatory resistance, hypertension, and left-heart hypertrophy by a cascade of events. If this hypothesis is true, the cause of essential hypertension is chronic respiratory and metabolic acidosis and RAAS activation. Preventing age-related intracellular acidosis through a non-hormonal way could prevent pathophysiological blood pressure elevation. It is a challenge to mitigate pCO2 level permanently and we, therefore, recommend a salt mixture of KH2PO4 and other Mg2+, K+, Ca2+ and phosphate salts to relieve the withdrawal symptoms in hypercapnia.
Keywords: Intracellular Acidosis; RAAS as a Feedback Mechanism; Salt-resistant Hypertension; Salt-Sensitive Hypertension; Weaning from Hypercapnia
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