Paul Saladino· MD
In the liver, there is a substance produced called angiotensinogen that is converted to angiotensin one by a substance called renin, which is produced by the kidneys. Renin will be released from the kidneys if the kidneys sense that blood pressure is low in a number of ways, at the level of arterioles, at the level of something called the JGA or the juxtaglomerular apparatus. Angiotensin one is converted to a more active form, angiotensin 2, by an enzyme called ACE, angiotensin-converting enzyme, found in the pulmonary and renal endothelium. Angiotensin 2 has many effects on the human body that are necessary for our survival in the setting of massive blood loss or dehydration, including increasing sympathetic activity. That is the fight or flight nervous system. Something that causes our blood pressure to be stable because our blood vessels will contract. Tubular sodium and chloride reabsorption, potassium excretion, water retention, that is primarily through the actions of aldosterone, and that is at the level of the kidney. You can see angiotensin 2 increases aldosterone secretion at the level of the adrenal gland. There is arteriolar vasoconstriction, increase in blood pressure, that is small arteries, and at the level of the pituitary gland, specifically the posterior pituitary, antidiuretic hormone or vasopressin is released, which causes water retention at the level of the kidneys. All of these are part of an in extremis situation for humans, for blood loss and dehydration. We will leverage this system in hypertension, but we are definitely cranking on levers that are not meant to be cranked on in this situation. We are pushing the gears and levers much past what they are meant to when we are not correcting the root cause of this problem.