Discussion in 'Alternative Therapies' started by xks201, Nov 14, 2012.
This research paper By Vanderbilt University researchers about POTS will give anyone interested in this topic some food for thought.
I think this figure (I wish I knew how to post it on this forum) Helps explain their current thinking about angiotensin, etc. in POTS....
Here is the abstract:
Heart Rhythm. 2011 Mar;8(3):422-8. Epub 2011 Jan 22.
Abnormalities of angiotensin regulation in postural tachycardia syndrome.
Mustafa HI, Garland EM, Biaggioni I, Black BK, Dupont WD, Robertson D, Raj SR.
Division of Clinical Pharmacology, Vanderbilt University School of Medicine, Nashville, Tennessee 37232-2195, USA.
Postural tachycardia syndrome (POTS) is a disorder characterized by excessive orthostatic tachycardia and significant functional disability. We previously reported that POTS patients have low blood volume and inappropriately low plasma renin activity (PRA) and aldosterone. In this study, we sought to more fully characterize the renin-angiotensin-aldosterone system (RAAS) to gain a better understanding of the pathophysiology of POTS.
The purpose of this study was to prospectively assess the plasma levels of angiotensin (Ang) peptides and their relationship to other RAAS components in patients with POTS compared with healthy controls.
Heart rate, PRA, Ang I, Ang II, Ang (1-7), and aldosterone were measured in POTS patients (n = 38) and healthy controls (n = 13) while they were consuming a sodium-controlled diet.
POTS patients had larger orthostatic increases in heart rate than did controls (52 ± 3 [mean ± SEM] bpm vs 27 ± 6 bpm, P = .001). Plasma Ang II was significantly higher in POTS patients (43 ± 3 pg/mL vs 28 ± 3 pg/mL, P = .006), whereas plasma Ang I and angiotensin 1-7 [Ang-(1-7)] were similar between groups. Despite the twofold increase of Ang II, POTS patients trended to lower PRA levels than did controls (0.9 ± 0.1 ng/mL/h vs 1.6 ± 0.5 ng/mL/h, P = .268) and lower aldosterone levels (4.6 ± 0.8 pg/mL vs 10.0 ± 3.0 pg/mL, P = .111). Estimated angiotensin-converting enzyme-2 (ACE2) activity was significantly lower in POTS patients than in controls (0.25 ± 0.02 vs 0.33 ± 0.03, P = .038).
Some patients with POTS have inappropriately high plasma Ang II levels, with low estimated ACE2 activity. We propose that these abnormalities in Ang regulation may play a key role in the pathophysiology of POTS in some patients.
Copyright © 2011 Heart Rhythm Society. Published by Elsevier Inc. All rights reserved.
PMID: 21266211 [PubMed - indexed for MEDLINE] PMCID: PMC3050076 Free PMC Article
Images from this publication.See all images (2) Free text
Publication Types, MeSH Terms, Substances, Secondary Source ID, Grant Support
I am just posting in xks201's personal signature below, which is the subject of this thread, for people that have their signature display turned off (or in case xks201 changes his signature in future, and then these details are lost):
I take it that you are aware of the Marshall Protocol treatment for ME/CFS, which uses high doses of the angiotensin II receptor blocker (ARB) drug Benicar (olmesartan) in its treatment plan.
Benicar is used in the Marshall Protocol for its activation of the nuclear vitamin D receptor inside each cell; but this drug's ability to block angiotensin II receptors may also have significance in ME/CFS treatment.
yes you are definately on to something here. Basically a subset of POTS patients seem to have elevated angiotensin II levels and paradoxically low aldosterone levels with perhaps faulty at-1 receptor vasoconstriction.
I read somewhere that some licorice constituents actually activate the at-1 receptor.
You can also try a Google Site Search
Separate names with a comma.