Artikel
Interactions between sodium chloride intake and AT1-receptor blockade on renal endothelin system gene expression in rats
Einflüsse der NaCl-Aufnahme und AT1-Rezeptor-Blockade auf die renale Genexpression von Komponenten des Endothelinsystems
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Autoren
Veröffentlicht: | 11. November 2004 |
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Gliederung
Text
The renal endothelin system participates in the regulation of body fluid and electrolyte homeostasis. We investigated if changes in NaCl intake affect renal cortical and medullary mRNA expression of ETA, ETB-receptors, and pre-pro-ET-1 by real time RT-PCR. Further, the responsiveness of expression levels to AT1-receptor blockade was tested. Male Sprague-Dawley rats were randomised to 6 groups (n = 8) receiving 1.8, 0.6 or 0.12 % NaCl diet with or without oral administration of losartan (30 mg/kg*d). Without losartan MAP was 110 mmHg in all diet groups. Losartan reduced MAP by 20 mmHg irrespective of NaCl intake (p < 0.001). Cortical ETA expression was not significantly altered by NaCl intake. Losartan reduced cortical ETA expression by 30 % in the 0.12 % NaCl diet but not in the other diet groups (p < 0.05). Medullary ETA expression was elevated by 30 % under 0.12% NaCl compared to 1.8 and 0.6 % NaCl (p < 0.05). This effect was abolished by losartan. ETB expression was not significantly affected by any intervention. Cortical pre-pro-ET1 expression showed a slight inverse relation to NaCl intake. Losartan administration increased cortical pre-pro-ET-1 expression on 1.8 and 0.6 % NaCl by 30-40% (p < 0.05) but was without effect on 0.12% NaCl. Medullary pre-pro-ET-1 expression was not affected by any intervention. Reduction in NaCl intake by factor 15 increases the dependence of cortical and medullary ETA but not ETB recpetor mRNA expression on AT1-receptor stimulation. Conversely, cortical expression of pre-pro-ET1 does not depend on AT1-receptor stimulation on low NaCl intake but can be increased by AT1 blockade with elevated NaCl intake.