ramakentesh Posted January 10, 2009 Report Share Posted January 10, 2009 And if so how did it affect your POTS? Quote Link to comment Share on other sites More sharing options...
Dawg Tired Posted January 10, 2009 Report Share Posted January 10, 2009 I'm on lisinopril. I take it at night because I tend to have "supine hypertension". It doesn't seem to have any effect on my symptoms. Quote Link to comment Share on other sites More sharing options...
firewatcher Posted January 10, 2009 Report Share Posted January 10, 2009 ACE inhibitors work via the Aldosterone-Renin system which could be screwed up in many POTS patients, I would be hesitant to use them (only because I have signs of hypovolemia and a demonstrated blunting of my aldosterone-renin reaction to upright posture, you may not have it.)From Wikipedia:ACE inhibitors, or inhibitors of Angiotensin-Converting Enzyme, are a group of pharmaceuticals that are used primarily in treatment of hypertension and congestive heart failure, in some cases as the drugs of first choice. Main article: Renin-angiotensin systemThis system is activated in response to hypotension, decreased sodium concentration in the distal tubule, decreased blood volume and renal sympathetic nerve stimulation. In such a situation, the kidneys release renin which cleaves the liver-derived angiotensinogen into angiotensin I. Angiotensin I is then converted to angiotensin II via the ACE in the pulmonary circulation as well as in the endothelium of blood vessels in many parts of the body.[1] The system in general aims to increase blood pressure.EffectsACE inhibitors lower arteriolar resistance and increase venous capacity; increase cardiac output and cardiac index, stroke work and volume, lower renovascular resistance, and lead to increased natriuresis (excretion of sodium in the urine).From Vanderbilt:Renin-aldosterone paradox and perturbed blood volume regulation underlying postural tachycardia syndrome. BACKGROUND: Patients with postural tachycardia syndrome (POTS) experience considerable disability, but in most, the pathophysiology remains obscure. Plasma volume disturbances have been implicated in some patients. We prospectively tested the hypothesis that patients with POTS are hypovolemic compared with healthy controls and explored the role of plasma renin activity and aldosterone in the regulation of plasma volume. METHODS AND RESULTS: Patients with POTS (n=15) and healthy controls (n=14) underwent investigation. Heart rate (HR), blood pressure (BP), plasma renin activity, and aldosterone were measured with patients both supine and upright. Blood volumes were measured with 131I-labeled albumin and hematocrit. Patients with POTS had a higher orthostatic increase in HR than controls (51+/-18 versus 16+/-10 bpm, P<0.001). Patients with POTS had a greater deficit in plasma volume (334+/-187 versus 10+/-250 mL, P<0.001), red blood cell volume (356+/-128 versus 218+/-140 mL, P=0.010), and total blood volume (689+/-270 versus 228+/-353 mL, P<0.001) than controls. Despite the lower plasma volume in patients with POTS, there was not a compensatory increase in plasma renin activity (0.79+/-0.58 versus 0.79+/-0.74 ng x mL(-1) x h(-1), P=0.996). There was a paradoxically low level of aldosterone in the patients with POTS (190+/-140 pmol/L versus 380+/-230 pmol/L; P=0.017). CONCLUSIONS: Patients with POTS have paradoxically unchanged plasma renin activity and low aldosterone given their marked reduction in plasma volume. These patients also have a significant red blood cell volume deficit, which is regulated by the renal hormone erythropoietin. These abnormalities suggest that the kidney may play a key role in the pathophysiology of POTS. PMID: 15781744 [PubMed - indexed for MEDLINE] Related Articles * Increased plasma angiotensin II in postural tachycardia syndrome (POTS) is related to reduced blood flow and blood volume. [Clin Sci (Lond). 2006]LOW FLOW POTS?????* Quote Link to comment Share on other sites More sharing options...
Claire Posted August 22, 2018 Report Share Posted August 22, 2018 I’m so sorry but I am having trouble understanding this. So, are ace inhibitors bad for autonomic neuropathy? Thank you. Quote Link to comment Share on other sites More sharing options...
Claire Posted August 22, 2018 Report Share Posted August 22, 2018 On 1/10/2009 at 3:59 AM, ramakentesh said: And if so how did it affect your POTS? What is a cycled vasoconstrictor-Clonidine? Quote Link to comment Share on other sites More sharing options...
bombsh3ll Posted August 22, 2018 Report Share Posted August 22, 2018 I've wondered about this too - my BP tends to run high. Increased stroke volume and cardiac output sound great, diuresis not so good! I am clinically in stage 2 hypovolaemic shock most of the time, but since I don't produce renin at all and barely detectable aldosterone, the suppression of this system may not be an issue in me. I would also like to hear anyone's experience with these. B x Quote Link to comment Share on other sites More sharing options...
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