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1 via NCC activation at the cost of increasing sodium retention.
2 igh plasma aldosterone and increased urinary sodium retention.
3 rough aldosterone binding and stimulation of sodium retention.
4 vity, sympathetic nervous activity and renal sodium retention.
5 y depressed plasma renin activity because of sodium retention.
6 nin-angiotensin-aldosterone system (RAAS) or sodium retention.
7 ase blood pressure, catecholamine levels, or sodium retention.
8 e rats several renal abnormalities encourage sodium retention.
9 de (ANP) characterize states of pathological sodium retention.
10 pulmonary hypertension, muscle weakness, and sodium retention.
11 ectly on the renal tubule is responsible for sodium retention.
12 sine is not responsible for vasodilation and sodium retention, (2) a sodium-retaining factor acting d
13 In contrast, severe CHF is characterized by sodium retention and coactivation of both ANP and the RA
16 hypertension have not been established, but sodium retention and excessive sympathetic tone are key
17 sodium transporters that are obligatory for sodium retention and hypertension in response to nitric
20 dysfunction and damage, leading to enhanced sodium retention and increased systemic vascular resista
24 However, whether T cells contribute to renal sodium retention and salt-sensitive hypertension is unkn
25 pressure-natriuresis relation in the kidney, sodium retention, and compensatory nocturnal natriuresis
26 inished renal potassium excretion, excessive sodium retention, and hypertension (pseudohypoaldosteron
28 pertension is most often caused by excessive sodium retention, and that spironolactone would therefor
29 creasing the circulatory flow, thus reducing sodium retention, ascites recurrence, and variceal bleed
30 ed by a suppressed plasma renin level due to sodium retention but manifests in eNOS uncoupling; howev
31 itors, muscle weakness by exercise training, sodium retention by diuretics and monitoring devices, my
35 n day 1 after surgery when transient maximal sodium retention developed and day 7 when rats returned
36 brain Galphai(2) proteins, animals exhibited sodium retention, global sympathoexcitation, and elevate
39 on of cGMP in response to ANP contributes to sodium retention in heart failure, but may be compensate
42 tenderness and bloating did not result from sodium retention in the luteal phase of the menstrual cy
46 As COX inhibition is often associated with sodium retention leading to edema and hypertension, pros
49 natriuretic peptide (ANP) and the excessive sodium retention seen in experimental nephrotic syndrome
50 ack patients also shows clinical features of sodium retention so we screened black people for the T59
51 adenosine in the peripheral vasodilation and sodium retention that occurs after partial portal vein l
52 ne conditions, portal hypertensive rats with sodium retention were hypotensive, with decreases in tot
53 unction of D1 receptors results in increased sodium retention which can potentially lead to the devel
54 tes results from sinusoidal hypertension and sodium retention, which is in turn secondary to vasodila
55 tes results from sinusoidal hypertension and sodium retention, which is, in turn, secondary to vasodi
56 tes results from sinusoidal hypertension and sodium retention, which, in turn, is secondary to vasodi
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