When constriction is the problem, not vasodilation
Just a reminder that nothing here is medical advice, it is general education only! Always approve any lifestyle or dietary changes with your providers.
When I first did my orthostatic test back in 2021 to obtain my POTS diagnosis, I remember my doctor being perplexed as to why, despite having more than a 30 BPM change in my heart rate upon standing, my blood pressure actually went up rather than down. My doctor was confused, because while my HR change fit the POTS profile, she told me she usually sees BP drop upon standing. Still, I was given a POTS diagnosis, and was sent along my merry way with a recommendation to include more salt and more compression. She said if I wanted to go on a beta blocker, I could try that.
I have had so many clients go through the exact same thing. What they experience looks and feels like POTS, however, it’s clear that their blood pressure tends to run aggressively high, or erratic, rather than classically low. The question is, why?
I believe that one potential explanation lies in the primary entry site of COVID into the cell: the ACE2 receptor. The ACE2 receptor is an incredibly important resource in the body. It is a critical regulator of the renin-angiotensin system, which is the hormone system that regulates the blood pressure, fluid balance and electrolyte homeostasis. One important job of this receptor is converting angiotensin II (a potent vasoconstrictor and pro-inflammatory peptide) into angiotensin 1-7, which has vasodilatory and protective effects. One problem when the virus enters via this receptor is that it can trigger damage to the ACE2 receptor and/or antibodies against this receptor, and the result is that you can get a buildup of Angiotensin II, which creates too much vasoconstriction. We need larger scale studies on this, but some preliminary small scale studies have startling outcomes:
In a cohort of 17 POTS patients, 12 (about 70%) showed elevated AT1R autoantibody activity, which can mimic or modulate the effects of Ang II
In a study of 38 POTS patients, plasma angiotensin II (Ang II) was significantly higher in the POTS group than in healthy controls
The tricky part is that as it stands today, it is difficult to test this theory. The tests are mostly taking place in research settings or specialty clinics, and are not yet FDA approved. However, I believe that one of the most important first steps to understanding whether or not this might apply to you is taking a deeper look at your blood pressure trends and your overall clinical picture. When I get a client that is consistently getting BP running high, rather than low, I am EXTREMELY cautious about adding additional sodium into the mix. This is tricky because once people get a POTS diagnosis, the next step is they are often recommended to increase sodium. This conversation is important to talk about because there are different subtypes of POTS; for those with more of a “hypovolemic” picture, where the BP clearly runs low upon standing, additional sodium is absolutely important. For people who do not fit that profile, I think we should be thinking twice before centering sodium, because I believe it has the potential to exacerbate the issue, if part of the issue is an elevation of Angiotensin II.
If your BP runs on the higher side, or if you have had other strange hypertension pictures pop up (pulmonary hypertension, intracranial hypertension, etc); it is worth considering addressing this potential issue. If you think this is you, the most important first step is reducing your sodium intake. Since angiotensin II can actually retain sodium, you don’t want to add insult to injury. Aerobic exercise is important, since regular aerobic activity increases ACE2 and decreases ACE/Ang II, improving blood pressure and antioxidant status. Of course this is a VERY nuanced since for some with Long COVID, aerobic exercise is contraindicated. Utah adapt can be an appropriate tool for many starting out with aerobic exercise, under supervision of a doctor of course (this is NOT medical advice). Certain foods like dairy, fish and soy may also upregulate ACE2 and counteract Angiotensin II. And of course, one of the most important things you can do is eat a high potassium diet; which does NOT mean powders, it means food, which is the safest and best way for our body to obtain potassium. Legumes and root veggies are the best sources, which is why I center these foods in Long COVID Academy and in my 1:1 work. Some people in this situation well with nitric oxide supplements, but of course this is NOT medical advice.
Another simplified way to think about this is that angiotensin II is your blood vessels making a clenched fist. I think to understand it can be helpful to physically and literally clench your fist: what happens when you squeeze your fist closed for 10 seconds, and then release it? You might notice more pain in your fingers, less flexibility in your fingers, paler fingers from less blood flow. We need to open that fist. Foods like potassium rich foods provide vasodilation: it’s like opening that fist up and letting the blood flow. Nitric oxide is opening the fist.
I am excited about potential therapies developing that can help address this problem, but in the meantime, I think starting somewhere (like the education listed above) can be a life changing place to start. If the usual POTS interventions don’t help you, it’s not your fault, you just don’t have that exact same issue going on.
Sources:
Yu, X., Li, H., Murphy, T., Nuss, Z., Liles, J., Liles, C., Aston, C., Raj, S., Fedorowski, A., & Kem, D. (2018). Angiotensin II Type 1 Receptor Autoantibodies in Postural Tachycardia Syndrome. Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease, 7. https://doi.org/10.1161/jaha.117.008351.
Mustafa, H., Garland, E., Biaggioni, I., Black, B., Dupont, W., Robertson, D., & Raj, S. (2011). Abnormalities of angiotensin regulation in postural tachycardia syndrome.. Heart rhythm, 8 3, 422-8 . https://doi.org/10.1016/j.hrthm.2010.11.009.
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