DISCLAIMER: This article in no way is recommending that you discontinue taking HTN pharmaceuticals. Medication management should always be coordinated with a medical professional. Homeostatic mechanisms are complex. Taking the drugs short-term versus long-term could have the opposite effect on ACE-II receptors. There are many other factors to consider in medication management including the potential rebound effects of lowering medication and the risk assessment of increasing your high blood pressure compared to the threat of the virus to name a few.
Most people infected with COVID-19 experience no more than mild Flu-like symptoms. Unfortunately, a small minority of patients react with life threatening severity to the virus. Emerging autopsy reports are showing that most non-survivors have a cardiovascular pre-existing condition, the most common being high blood pressure (HTN). HTN is found in between 1/3 and 1/2 patients admitted to hospitals in tracking studies of COVID-19 infection1. This article will explain the physiology of why this vulnerable group, those with high blood pressure, are more likely react to the virus severely.
The Renin-angiotensin-aldosterone system (RAAS) is a hormonal pathway responsible for regulating blood pressure as well as fluid, and electrolyte balance in the body. RAAS activates when pressure receptor cells in the kidney sense that blood pressure is too low. This initiates a hormonal cascade that travels from the kidneys to the lungs and heart that constricts arteries and increases vascular fluid throughout the body. The RAAS ensures vital organs are sufficiently perfused with blood by increasing blood pressure.
Most high blood pressure pharmaceuticals work by blocking a part of the RAAS. This limits your body’s ability to raise blood pressure. ACE (the class of drugs that end in ‘opril’) inhibits the enzyme that converts the hormone angiotensin I -> angiotensin II. ARB (the class of drugs that end in ‘artan’) blocks the hormone angiotensin II from attaching to its cellular receptor.
Over time, the body responds to inhibition of the RAAS by increasing the expression of receptors and enzymes that promote the RAAS. This is an example of negative feedback, regulatory loops that stabilize biological systems. Their purpose is to swing back to homeostasis (a physiological set point) when things deviate too far. For example, our body temperature hovers around 98.6 F, our blood pH hovers around 7.40 due to negative feedback loops that return to these homeostatic set points.
Homeostasis is like a balance scale. If a weight is applied to one side, the body responds by applying a counterweight. The scales may rock back and forth a bit during this process until it eventually returns to a point of balance. That is, until another new weight is added, and the process starts all over again.
A very important cellular receptor amidst this pandemic is ACE-II, because of its relationship to COVID-19. ACE-II, in additional to being part of the RAAS, is also the receptor that the COVID-19 virus uses to enter a cell. Experimental models have shown that ACE-II receptors are increased for those taking ACE and ARB pharmaceuticals2 likely due to negative feedback loops. This means that high blood pressure patients have more entry ways for the virus to infect cells. Incidentally, ACE-II receptors are also increased in diabetes patients, the second most likely group after hypertension to be severely affected by COVID-193.
Once cells are infected with the virus, the immune system activates an inflammatory process targeted at the infected cells. While the immune system is very effective at viral elimination, it also creates collateral tissue damage. Tissue damage in the arm might not be too concerning – your arm can nearly double in size temporarily without any lasting damage; yet, even moderate tissue damage around vital organs can be fatal.
COVID-19 unfortunately infects tissue that surround vital organs meaning that the tissue damage caused by the immune response to the virus could be fatal. Again, this is because COVID-19 infects cells with ACE-II receptors. That receptor is found in cells along the RAAS3 that line vital organs including lungs, heart, and kidney. Your immune system, while fighting the virus around these organs, may create enough tissue damage to weaken your breathing and pulse. In other words, it is the response to the virus, not the virus itself that can prove deadly.
This is an informational article to help you understand the importance of optimizing the function of your cardiovascular and immune system in preventing a severe response to COVID-19.
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