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Do these G.I.-related gurgling sounds happen right after you eat, or can they happen several hours later? I don't know anything about the digestive process.

I believe I have blood pooling in my abdomen. Although I think it is from POTS, I frequently heart gurgling noises from my stomach and wonder whether they could be from ascites due to heart failure or cirrhosis. My concerns about ascites were based on my assumption that blood would have a higher "viscosity" (or whatever the term is) and would not be prone to gurgling noises, whereas the water (or whatever fluid) from ascites would have a lower viscosity and be more prone to squishing around. So my question is whether other POTS patients who have abdominal pooling hear gurgling sounds.

I am currently doing some tests on my own to explore my POTS symptoms. Two of the variables I see referenced are Nitric Oxide and the Renin-Angiotensin-Aldosterone system. For nitric oxide, I don't see any tests available in my Google searching. For the RAS system, I see blood tests for Renin & Aldosterone, but I don't see tests for Angiotensin II. I only see tests for "Angiotensin-Converting Enzyme (ACE)". How are these tested? Can I get them tested without going to a doctor?

I don't know as much as some other people about POTS theories, but I have been doing some research about CRP & inflammation. Here are a couple of potentially useful links that I found: http://www.beyotime.com/reference/aj516-2-aj518-2-am071-am076-ref3.pdf Excerpt: "Conclusion: The present study demonstrates that AngII has ability to induce CRP expression in HAECs [human aortic endothelial cells] through AT1-ROS-ERK1/2 and JNK-NF-kB signal pathway, which strengthens understanding of the proinflammatory and proathroscerotic actions of AngII." http://hyper.ahajournals.org/cgi/content/short/HYPERTENSIONAHA.109.140608v1 Excerpt: "In conclusion, CRP is not only a biomarker but also a mediator in Ang II–mediated cardiac remodeling. Enhanced upregulation of the Ang II type I receptor and activation of the transforming growth factor-{beta}/Smad and nuclear factor-{kappa}B signaling pathways may be the mechanisms by which CRP promotes cardiac fibrosis and inflammation under high Ang II conditions."