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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Dietary sodium regulates angiotensin AT1a and AT1b mRNA expression in mouse brain.

Previous results showed that angiotensin (Ang) AT1a and AT1b receptor mRNA are expressed in mouse hypothalamus (HYP), brainstem (BS) and anterior pituitary (PIT). To extend these findings, we developed a real-time polymerase chain reaction (PCR) method to differentiate and quantify Ang AT1a and AT1b mRNA in mouse brain. An experiment was conducted in male C57Bl/6J mice to determine the effects of low and high dietary salt (0.04 or 8% NaCl for 2 weeks) on mRNA expression. Physiological measurements showed that high salt increased water intake (15.1 +/- 0.6 ml/day), whereas low salt decreased water intake (3.2 +/- 0.1 ml/day). There were no significant changes in body weight, hematocrit or plasma osmolality. Real-time PCR was effective in distinguishing AT1a and AT1b receptor mRNA. The PCR efficiencies for AT1a, AT1b and 18S ribosome were tested to be identical, making it possible to quantify mRNA levels. There were differences in angiotensin receptor expression, related to diet and brain region. In hypothalamus, both the high salt and low salt diet decreased AT1a expression (to 63 +/- 4% and 62 +/- 1%), although there were no changes in AT1b. In brainstem, there was a marked increase in AT1a (to 365 +/- 60%) and AT1b (to 372 +/- 23%) after high salt, although there was only a marked decrease for AT1b (to 23 +/- 5%) after low salt. In anterior pituitary, both high salt and low salt diet increased AT1a expression (to 152 +/- 8% and 123 +/- 9%), although there were no changes in AT1b. Results document that both AT1 receptor subtypes are present in mouse hypothalamus, brainstem and anterior pituitary, and that there is differential regulation of expression in response to changes in dietary salt.[1]


  1. Dietary sodium regulates angiotensin AT1a and AT1b mRNA expression in mouse brain. Chen, Y., Liu-Stratton, Y., Hassanain, H., Cool, D.R., Morris, M. Exp. Neurol. (2004) [Pubmed]
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