Resch, Markus and Bergler, Tobias and Fredersdorf, Sabine and Griese, Daniel P. and Weil, Joachim and Kreuzer, Peter and Brunner, Sabine and Riegger, Guenter A. J. and Luchner, Andreas and Endemann, Dierk H. (2010) Hyperaldosteronism and altered expression of an SGK1-dependent sodium transporter in ZDF rats leads to salt dependence of blood pressure. HYPERTENSION RESEARCH, 33 (10). pp. 1082-1088. ISSN 0916-9636,
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This study was designed to test whether altered aldosterone-related sodium handling leads to salt-sensitive blood pressure in diabetes and thus may exaggerate end-organ damage. Zucker diabetic fatty (ZDF) rats, a model of type 2 diabetes, and Zucker lean (ZL) rats, as euglycemic controls, were divided into groups receiving normal (0.28%) (ZDF+N, ZL+N) and high-salt (5.5%) diets (ZDF+S, ZL+S) for 10 weeks. Renal mRNA expression of serum-and glucocorticoid-inducible kinase 1 (SGK1) and sodium transporters (for example, the epithelial sodium channel-alpha, ENaC alpha) were measured by quantitative reverse transcriptase-PCR. Vascular hypertrophy (media-to-lumen ratio, M/L) in mesenteric resistance arteries was assessed using a pressurized myograph. Systolic blood pressure (SBP) was significantly higher in ZDF+S vs. ZDF+N (146 +/- 2 vs. 133 +/- 3 mm Hg; P < 0.05), whereas there was no difference between ZL+S and ZL+N (151 +/- 3 vs. 147 +/- 3 mm Hg). Plasma sodium concentration was higher in ZDF+S vs. ZDF+N, whereas there was no difference between ZL+S and ZL+N. Plasma aldosterone concentration (PAC) was higher in ZDF+N as compared with ZL+N (191 +/- 23 vs. 95 +/- 35 pg ml(-1); P<0.05). PAC decreased to zero in ZL+S, which was not the case in ZDF+S (0 +/- 0 vs. 37 +/- 2 pg ml(-1)). Salt loading decreased the mRNA expression of SGK1 in euglycemic controls (ZL+S 0.58 +/- 0.2 vs. ZL+N 1.05 +/- 0.05; P 0.05), whereas it significantly increased SGK1 expression in diabetic rats (ZDF+S 1.75 +/- 0.15 vs. ZDF+N 0.92 +/- 0.07; P<0.01). ENaCa mRNA expression paralleled these changes. The M/L of mesenteric resistance arteries was not different between ZDF+N and ZL+N. High salt significantly increased the M/L in ZDF+S vs. ZDF+N, but not in ZL+S vs. ZL+N. Systolic blood pressure in this model of type 2 diabetes mellitus is salt sensitive, leading to marked vascular remodeling. The underlying pathophysiological mechanism may be inappropriately high levels of aldosterone and up-regulation of SGK1-dependent renal sodium transport by ENaCa, leading to net increased sodium retention. Hypertension Research (2010) 33, 1082-1088; doi:10.1038/hr.2010.132; published online 22 July 2010
| Item Type: | Article |
|---|---|
| Uncontrolled Keywords: | OBESE ZUCKER RATS; EPITHELIAL NA+ CHANNEL; DIABETES-MELLITUS; SIGNALING PATHWAY; HYPERTENSIVE-RATS; DIETARY-SODIUM; ALDOSTERONE; SERUM; ENAC; KINASE; EnaC; salt-sensitive blood pressure; SGK1 |
| Subjects: | 600 Technology > 610 Medical sciences Medicine |
| Divisions: | Medicine > Lehrstuhl für Innere Medizin II |
| Depositing User: | Dr. Gernot Deinzer |
| Date Deposited: | 13 Jul 2020 05:35 |
| Last Modified: | 13 Jul 2020 05:35 |
| URI: | https://pred.uni-regensburg.de/id/eprint/24076 |
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