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1 ce often occur in concert with elevations in plasma aldosterone.
2 (4) These mice show higher levels of the plasma aldosterone.
3 decreased renal Na(+) avidity and increased plasma aldosterone.
4 ore than 50% without changing PCa++, PK+, or plasma aldosterone.
5 phenotype, except for a 2.5-fold increase in plasma aldosterone.
6 re (94 +/- 2 vs. 89 +/- 2 mm Hg, P = 0.002), plasma aldosterone (149 +/- 18 vs. 109 +/- 10 pmol/L, P
7 - 9 mg/d) and thrombotic microangiopathy and plasma aldosterone (18 +/- 18 pg/ml) remained low but da
8 tassium (4.3+/-0.5 to 4.7+/-0.6 mmol/L), and plasma aldosterone (281 [198-431] to 351 [241-494] ng/L)
10 c, inappropriate (dietary Na+) elevations in plasma aldosterone (ALDO) and a catabolic state that inc
14 of sodium in their feces and exhibited high plasma aldosterone and increased urinary sodium retentio
19 increase of plasma potassium (p < 0.02), but plasma aldosterone, angiotensin II (ANGII), and renin ac
20 ided clinical validation for the lowering of plasma aldosterone as a viable approach to modulate bloo
27 ations nearly 20-fold, which correlated with plasma aldosterone concentration and urinary Na/K ratio.
28 nd no difference in plasma renin activity or plasma aldosterone concentration between salt-fed wild-t
29 tensive patient, a serum potassium level and plasma aldosterone concentration to plasma renin activit
30 f hypertension, higher preoperative ratio of plasma aldosterone concentration to plasma renin activit
32 dditional measurement of serum potassium and plasma aldosterone concentration-plasma renin activity r
33 KNG1]: P=0.001 for plasma renin, P=0.024 for plasma aldosterone concentration; and rs4253311 with P<0
37 eart failure produces sustained reduction in plasma aldosterone, consistent with the observed signifi
39 ke (120 +/- 124 versus 580 +/- 442 pg/ml for plasma aldosterone, group 1 versus group 2, P = 0.03, an
40 n activity [PRA] <=1.0 ng/mL/h) and elevated plasma aldosterone (>=1.0 ng/dL) were enrolled, with sub
42 ensate for impaired ENaC activation, rise in plasma aldosterone in response to low-salt diet was enha
57 ffects of an angiotensin receptor blocker on plasma aldosterone levels in patients with NYHA class II
59 In control mice, rosiglitazone did not alter plasma aldosterone levels or protein expression of ENaC
60 ical studies have demonstrated that elevated plasma aldosterone levels predict the development of ins
61 duced-potassium diet (rescue diet), although plasma aldosterone levels remained significantly increas
62 asurements of adrenal CYP11B2 expression and plasma aldosterone levels showed that increases in endog
63 was increased, and plasma renin activity and plasma aldosterone levels were decreased after the HS di
64 enin concentrations were modestly higher and plasma aldosterone levels were lower in Sglt2(-/-) mice.
68 ing the intron conversion have (a) increased plasma aldosterone levels, (b) increased hCYP11B2 mRNA a
69 Systolic BP (SBP), 24-h protein excretion, plasma aldosterone levels, 24-h urinary aldosterone excr
71 1, we investigated the relationship between plasma aldosterone levels, ethanol self-administration a
72 hs accompanied with proportionate changes in plasma aldosterone levels, whereas plasma volumes ranged
79 ted thrombotic microangiopathy and decreased plasma aldosterone (<16 versus 710 +/- 91 pg/ml; P < 0.0
80 oncentration (P=0.01) and a trend for higher plasma aldosterone (P=0.06), but measures of home BP, pl
83 negatively and significantly correlated with plasma aldosterone (r=-0.38, P=0.0006), 24-hour urinary
85 ommon nonpressor effects included changes in plasma aldosterone, renal function, cardiac variables, a
87 otassium intake, Tmprss2(-/-) mice increased plasma aldosterone significantly more than wild-type mic
88 ldosterone (r=-0.49, P<0.0001), and ratio of plasma aldosterone to plasma renin activity (r=-0.43, P<
89 ely evaluated with an early-morning ratio of plasma aldosterone to plasma renin activity and 24-hour
90 chemical and clinical success (reductions in plasma aldosterone to renin ratio and blood pressure 6 m
93 were observed in plasma renin concentration, plasma aldosterone, urine vasopressin, or urine PGE(2) b
97 haracteristic of primary aldosteronism), but plasma aldosterone was only elevated in male animals.
101 in signaling elevated CYP11B2 expression and plasma aldosterone, whereas deficiency in leptin or lept