17beta-estradiol deficiency reduces potassium excretion in an angiotensin type 1 receptor-dependent manner.

17beta-estradiol deficiency reduces potassium excretion in an angiotensin type 1 receptor-dependent manner. Research Abstract Details 

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17beta-estradiol deficiency reduces potassium excretion in an angiotensin type 1 receptor-dependent manner. Abstract Text:

Hong Ji,Wei Zheng,Celine Falconetti,Darren M Roesch,Susan E Mulroney,Kathryn Sandberg,

This study examined the effects of ovariectomy (OVX) and 17beta-estradiol (E(2)) replacement (OVX + E(2)) on renal function in Sprague-Dawley rats. OVX caused a 40% decrease in the fractional excretion of potassium (FE(K(+))) that was prevented by E(2) replacement [Sham, 24.2 +/- 2.9%; OVX, 14.5 +/- 2.1% (P < 0.05 vs. OVX + E(2)); and OVX + E(2), 26.2 +/- 2.7%; n = 7-11] and that corresponded to significant increases in plasma potassium [(in mmol/l): Sham, 3.15 +/- 0.087; OVX, 3.42 +/- 0.048 (P < 0.05 vs. OVX + E(2)); and OVX + E(2), 3.19 +/- 0.11; n = 7-11]. No effects of OVX were detected on plasma levels of sodium and aldosterone. Angiotensin II type 1 receptor (AT(1)R) densities in ovariectomized rats were 1.4-fold and 1.3-fold higher in glomerular [maximum binding capacity (B(max); in fmol/mg protein): Sham, 482 +/- 21; OVX, 666 +/- 20 (P < 0.05 vs. OVX + E(2)); and OVX + E(2), 504 +/- 26; n = 7-11] and proximal tubular [B(max) (in fmol/mg protein): Sham, 721 +/- 16; OVX, 741 +/- 24 (P < 0.05 vs. OVX + E(2)); and OVX + E(2), 569 +/- 23; n = 7-11] membranes compared with E(2) replete animals, respectively. Both the angiotensin-converting enzyme inhibitor captopril and the AT(1)R antagonist losartan prevented the OVX-induced decrease in the FE(K(+)) and the increase in renal AT(1)R densities, suggesting that E(2) deficiency reduces potassium excretion in an ANG II/AT(1)R-dependent manner. These findings may have implications for renal function in postmenopausal women as well as contribute to the reasons underlying the age-induced increase in susceptibility to hypertension-associated disease in women.

17beta-estradiol deficiency reduces potassium excretion in an angiotensin type 1 receptor-dependent manner. Publishing Authors By Initials

H Ji,W Zheng,C Falconetti,DM Roesch,SE Mulroney,K Sandberg,

For similar proteins: membrane proteins: receptors, cell surface: receptors, g-protein-coupled: receptors, angiotensin: receptor, angiotensin, type 1 research abstracts see: proteins: membrane proteins: receptors, cell surface: receptors, g-protein-coupled: receptors, angiotensin: receptor, angiotensin, type 1 research

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17beta-estradiol deficiency reduces potassium excretion in an angiotensin type 1 receptor-dependent manner. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: American journal of physiology. Heart and circulat

VOLUME: 293

Page Numbers: H17-22

Journal Abbreviation: Am. J. Physiol. Heart Circ. Ph

ISSN: 0363-6135

DAY: 20

MONTH: 04

YEAR: 2007

17beta-estradiol deficiency reduces potassium excretion in an angiotensin type 1 receptor-dependent manner. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 100901228

17beta-estradiol deficiency reduces potassium excretion in an angiotensin type 1 receptor-dependent manner. Keywords Mesh Terms:

KEYWORDS: Receptor, Angiotensin, Type 1

MESH TERMS: metabolism

Chemical & Substance for Abstract: 17beta-estradiol deficiency reduces potassium excretion in an angiotensin type 1 receptor-dependent manner. Information

Substance Name: Potassium

Registry Number: 7440-09-7

Grant and Affiliation Information for 17beta-estradiol deficiency reduces potassium excretion in an angiotensin type 1 receptor-dependent manner.

AFFILIATION: Center for the Study of Sex Differences, Georgetown University, 4000 Reservoir Road NW, Washington, DC 20057, USA. jih@georgetown.edu

Country: United States

AGENCY: United States NIA

GRANT: AG 19121

ACRONYM: AG

MEDLINETA: Am J Physiol Heart Circ Physio

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