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1 POTS and NCS differ in tonic cardiac sympathetic functio
2 POTS may be associated with increased limb blood flow ("
3 oneal muscle sympathetic nerve activity in 9 POTS patients and 9 control subjects at rest and during
5 tudy addressed whether patients with COI and POTS or NCS have neurocirculatory abnormalities during s
6 Volume-pressure relations of controls and POTS patients with normal P(v) and high P(v) were not di
9 Disorder Treatment Study for Young Children [POTS Jr]) conducted at 3 academic medical centers betwee
10 (MSN) discharge characteristics in 12 female POTS patients and in 9 male and 12 female control subjec
12 ) combined with iontophoresis in 15 low-flow POTS patients, 17 normal-flow POTS patients, and 13 heal
13 rn of thermal hyperemia response in low-flow POTS subjects during saline administration resembled the
15 ycardia syndrome (POTS), designated low-flow POTS, is associated with decreased peripheral blood flow
17 decreased peripheral blood flow in low-flow POTS, we performed experiments using laser-Doppler flowm
19 in 15 low-flow POTS patients, 17 normal-flow POTS patients, and 13 healthy reference volunteers varyi
24 ion to the increase in total MSN activity in POTS patients compared with female control subjects, and
25 tion was shifted toward larger amplitudes in POTS patients (p < 0.005), consistent with increased sym
31 o the total activity increase was greater in POTS patients than in female (p < 0.05) and male (p < 0.
36 and mRNA expression were 2-3 times lower in POTS fibroblasts, and choline uptake was reduced 60% (P
38 ed sympathetic outflow significantly more in POTS patients than in controls despite a similar BP decr
39 ting diastolic function was mostly normal in POTS before training, though diastolic suction was impai
40 ulatory control during exercise is normal in POTS; and (b) that physical 'reconditioning' with exerci
42 At rest, the burst frequency was similar in POTS patients and controls (18.1+/-6.2 and 20.1+/-7.9 bu
43 Mean cardiac norepinephrine spillover in POTS (171+/-30 pmol/min, N=16) was higher and in NCS (62
44 ociated with a reduced stroke volume (SV) in POTS, and that the high heart rate (HR) observed at rest
58 OI) occurs in postural tachycardia syndrome (POTS) and in some individuals with repeated neurocardiog
60 e postural orthostatic tachycardia syndrome (POTS) and that exercise training improves this syndrome.
61 e postural orthostatic tachycardia syndrome (POTS) are primarily premenopausal women, which may be at
62 Patients with postural tachycardia syndrome (POTS) experience considerable disability, but in most, t
67 e postural orthostatic tachycardia syndrome (POTS) report fluctuations in orthostatic tolerance throu
68 racterized by postural tachycardia syndrome (POTS) with exaggerated tachycardia, orthostatic symptoms
69 ne variant of postural tachycardia syndrome (POTS), designated low-flow POTS, is associated with decr
72 h postural orthostatic tachycardia syndrome (POTS), who presented with low plasma choline and betaine
82 udied 12 patients 13 to 19 years of age with POTS and defective leg vasoconstriction and 13 age-match
83 ng of sympathetic fiber loss associated with POTS, may contribute to the predisposition to and greate
84 ow level of aldosterone in the patients with POTS (190+/-140 pmol/L versus 380+/-230 pmol/L; P=0.017)
85 g/kg per minute) for 1 hour in patients with POTS (n=15) and healthy controls (n=13) in the supine po
87 METHODS AND In protocol 1, patients with POTS (n=54) underwent acute drug trials of propranolol 2
89 odium excretion was similar in patients with POTS and controls (-49+/-12 versus -60+/-16 mEq/g creati
91 ely tested the hypothesis that patients with POTS are hypovolemic compared with healthy controls and
92 re asymptomatic during HUT and patients with POTS are more likely to be symptomatic than patients wit
93 ly increased in the forearm in patients with POTS but was increased in the calf (9.3+/-2.2 versus 5.7
94 upine and upright positions in patients with POTS compared with control subjects (P=0.01, upright leg
95 ine was significantly lower in patients with POTS compared with controls (10.1+/-1.2 versus 16.8+/-1.
97 n response to Ang II infusion, patients with POTS had a blunted increase compared with controls in me
102 We have previously found that patients with POTS have increases in plasma angiotensin II (Ang II) th
108 ilarly with Ang II infusion in patients with POTS versus controls (-166+/-20 versus -181+/-17 mL/min
110 ite the lower plasma volume in patients with POTS, there was not a compensatory increase in plasma re
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