It breaks down angiotensin to angiotensin (1-9) and angiotensin II into angiotensin (1-7). The first ACE enzyme (discovered in 1956) breaks down angiotensin into angiotensin II and angiotensin.ĪCE-2 has been referred to as the “ protective arm of the renin-angiotensin system“. The ACE enzymes (ACE and ACE-2) break down angiotensin in different ways. Levels of the ACE-2 enzyme appear to be low in ME/CFS and POTS That was a timely finding as the ACE-2 enzyme had only been discovered seven years earlier. In “ Abnormalities of Angiotensin Regulation in Postural Tachycardia Syndrome“, Vanderbilt researchers suggested they’d found a reason for the high Ang II levels – reduced activity of the angiotensin converting enzyme 2 (ACE-2) that breaks down angiotensin. ACE-2 Enzymeįive years later, a deeper dive into the renin-aldosterone paradox produced more answers – and more questions.
With all that sympathetic nervous system activity going on, the low blood volume POTS patients should have high blood pressure – instead, they often have the opposite. High Ang II levels also appear to be responsible for the defects in the vasodilation in the small blood vessels in the skin, which sometimes cause acrocyanosis (bluish color) in the hands and feet. It might simply be providing the amount of blood needed to fill the reduced blood vessel capacity that was present. The body senses the amount of space available in the blood vessels and seeks to provide the correct amount of blood. Narrowing of the blood vessels (increased vasoconstriction) caused by Ang II could itself cause low blood volume simply by reducing the total volume of the blood the vessels could carry. Since Ang II acts like a neurotransmitter in the brain, it could have multiple effects there as well. High Ang II levels potentially set the stage for a ramped up fight/flight system, narrowed blood vessels, inflammation and possibly reduced blood flows to the brain. Increased peroxynitrite, then, can reduce the levels of nitric oxide – an important vasodilator. It also jacks up oxidative stress levels through the formation of the superoxide radical and ultimately peroxynitrite. Ang II ramps up vasoconstriction (narrowing) in the blood vessels by prompting the release of norepinephrine from the sympathetic nerves. At high levels it can have some decidedly negative effects. The big news, though, was that instead of having low Ang II levels, the low blood volume and low-flow POTS patients had dramatically increased Ang II levels (2-3 times normal), as well as low renin levels.Īngiotensin II does more than increase blood volume. Very high levels of Ang II may be wreaking havoc in POTS and ME/CFS It was decreased in patients they called low-flow POTS, but not in two other subgroups.Īngiotensin enzyme in conjunction with angiotensin. In a 2006 paper, Stewart and Medow found that low blood volume was not universal at all in POTS. The authors believed that reduced angiotensin levels were probably responsible, but also suggested the damaged autonomic nerves in the kidney could be a factor. With that, the “renin-aldosterone paradox” had been born. Given the “profound” low blood volume found, both renin and aldosterone levels should have been dramatically increased, but the opposite was happening they were both decreased in postural orthostatic tachycardia syndrome (POTS). (Aldosterone secretion can also be stimulated by potassium, adrenocorticotropic hormone (ACTH), and low sodium levels in the blood (hyponatremia).) Angiotensin II then stimulates the production of aldosterone – the main factor – which regulates blood pressure, plasma sodium and potassium levels and blood volume. If blood volume is low, renin activity should be high.įirst, renin stimulates angiotensin II, which increases blood pressure and stimulates sodium absorption. Renin is the first leg of the renin-angiotensin-aldosterone system (RAAS) that’s designed to deliver optimal blood volume levels.
The renin-angiotensin-aldosterone system that regulates blood volume presents a paradox in ME/CFS and FM.
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