SARS-CoV-2 has caused a pandemic coronavirus disease 2019 (COVID-19), claiming over a million worldwide lives of people among whom those with cardiovascular disease or hypertension are over-represented. Understanding the mechanism by which coronavirus threatens human health is vital for reducing the current disease burden and even for preventing future attacks. Inspired by the temporal relationship between three coronavirus outbreaks in humans since 2000 and hypertension medications gaining popularity since 2000, we discuss here how hypertension medications might contribute to the COVID-19 pandemic and mortality with a focus on inhibitors of the renin-angiotensin-aldosterone system (RAAS). The fact that RAAS inhibitors increase angiotensin converting enzyme-2 (ACE2) expression in respiratory epithelial cells, the kidneys and heart has stirred a surge of interest in the discussion of the role of RAAS inhibitors in COVID-19 disease, all related to ACE2-mediated effects [1–5]. Here, we abstain from contributing further to this extensive discussion, but expand this discussion beyond ACE2 and centre on how RAAS blockade influences human interaction with SARS-CoV-2 by altering acid-base balance. This expansion is based on our previous experimental work conducted on aldosterone deficient mice  and on the fact, supported by accumulated groundwork in physiology, that acid-base homeostasis is maintained by the coordinated work of kidneys and lungs, and is vital for normal physiology and health. RAAS evolved to facilitate humans’ adaptation to land life by conserving salt and water in the intestine and kidney, and facilitating renal acid and other water-soluble waste elimination. As renal acid-excretion effects are largely dependent on the RAAS, inhibiting renal salt absorption by RAAS inhibitors in attempt to reduce blood pressure also slows renal acid elimination (see fig. 1 below).