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1 out mice, suggesting a facilitation in renal Na+ retention.
2 olume therefore appears to be the signal for Na+ retention.
3          How overexpression of WNK1 leads to Na(+) retention and hypertension is not entirely clear.
4  an important element of aldosterone-induced Na(+) retention and hypertension.
5  novel therapeutic target for treating renal Na(+) retention and hypertension.
6    Renal AT2R activation with C-21 prevented Na(+) retention and lowered blood pressure in the angiot
7          Intrarenal AT2R activation prevents Na(+) retention and lowers blood pressure in angiotensin
8 rats, Ang II infusion increased both sodium (Na(+)) retention and BP on day 1, and BP remained elevat
9 ffective as spironolactone in overcoming the Na+ retention and lowering blood pressure.
10 sion, peripheral vasodilatation (PVD) causes Na+ retention as a result of vascular underfilling.
11  impaired AT(2)R signaling and renal sodium (Na(+)) retention by utilizing the selective AT(2)R agoni
12 r Na+ retention ceases, it may contribute to Na+ retention by decreasing central blood volume.
13 tal peripheral resistance remains decreased, Na+ retention ceases after central blood volume is norma
14                  Although PVD persists after Na+ retention ceases, it may contribute to Na+ retention
15 on 4A (the first exon for KS-WNK1) exhibited Na(+) retention, elevated blood pressure on a high-Na(+)
16 rmal or high-Na diet and prevented excessive Na retention in salt-loaded CD ET-1 KO mice.
17 tential for DCT hypertrophy to contribute to Na(+) retention in a hypertensive condition.
18 , often neglected component of this trait is Na(+) retention in vacuoles.
19 etermine the role of central blood volume in Na+ retention in portal hypertensive rats.
20 ine whether escape from aldosterone-mediated Na retention is associated with decreased abundance of o
21 ease or response may still contribute to the Na+ retention of low-renin hypertension.
22 nistration of C-21 prevented Ang II-mediated Na(+) retention on day 1, induced continuously negative
23 )-exchanger-3 and Na(+)/K(+)ATPase, prevents Na(+) retention resulting in negative cumulative Na(+) b
24 HKalpha(1)(-/-)) resulted in greater urinary Na(+) retention than observed in either wild-type mice o
25 ion of central blood volume and cessation of Na+ retention were observed despite persistent PVD.