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Postural Orthostatic Tachycardia Syndrome (POTS) is a clinical syndrome characterized by the presence of tachycardia in the absence of orthostatic hypotension; symptoms of orthostatic intolerance (presyncope and syncope) are present secondary to autonomic dysfunction (1). It is thought that one of the implications for POTS involves plasma volume disturbances leading to blood pooling. The Renin Angiotensin Aldosterone System (RAAS) is one system that assists in plasma volume regulation (2). In this study we hypothesized that these disturbances are brought about by an inactivation of RAAS. This was done by retrospectively reviewing the medical records of POTS patients. In these patients, diagnosis of POTS was established by an increase in Heart Rate of over 30 bpm within 10 minutes of tilt. Stroke Volume was used as a measure of volume disturbances; those POTS patients whose stroke volumes had not increased by the End of the Tilt as compared to their 6 minute supine baseline were considered to have an inactivation of RAAS. Our total sample of POTS patients numbered at 447, out of which 417 patients had lower stroke volumes at the end of their tilt table tests when compared to their baseline; this makes for 92.87% of our POTS Patient Sample. The average Stroke Volume at the 6 minute mark was calculated to be 74.67; the average stroke volume at the end of the tilt table test (30 minutes) was calculated to be 46.33 mL; . The results seen in this study show that more than 90% of our POTS Patient Sample there is no recovery of the stroke volume by the end of the tilt table test, this volume disturbance can be the result of decreased RAAS activation. This observation is supported by the difference found between average stroke volumes seen at 6 minute baseline and at 30 minutes of tilt. In normal individuals, we should see an increase in stroke volume at the end of the tilt as RAAS is activated. However, as patients with POTS are known to have lower plasma volumes (2), compounded with the inactivation of RAAS; the resulting hypovolemia will amplify the symptoms of POTS, increasing their severity. These patients should respond well to fludrocortisone, as there will be a correction of hemodynamic impairments (RAAS inactivation) leading to symptomatic relief (3). Further studies and analyses are needed to look into the levels of Renin and Aldosterone at Baseline & at Tilt, as well as the effects of fludrocortisone on such patients with RAAS inactivation. References:(1) Satish R. R., Circulation. 2013. June 11; 127(23): 2336-2342.(2) Satish R. R. et al., Circulation. 2005. March 2; 111(13): 1574-1582. (3) Freitas. J et al., Clin Auton Res. 2000. October; 10(5): 293-303. Unless otherwise noted, all abstracts presented at ENDO are embargoed until the date and time of presentation. For oral presentations, the abstracts are embargoed until the session begins. Abstracts presented at a news conference are embargoed until the date and time of the news conference. The Endocrine Society reserves the right to lift the embargo on specific abstracts that are selected for promotion prior to or during ENDO.