Low dietary salt intake (0.2 mg/g) transiently decreased AT1A receptor mRNA in most organs but increased AT1B receptor mRNA in the adrenal gland, showing an organ- and subtype-dependent response.
Dietary salt reduction differentially modulates AT1 receptor subtype gene expression in an organ- and time-dependent manner in rats, potentially aiding adaptation to low salt intake.
Abstract This study aimed to characterize the influence of dietary salt intake on the gene expression of angiotensin II type 1 (AT 1 ) receptor subtypes in different organs. Male Sprague-Dawley rats were fed low salt (0.2 mg/g), normal salt (6 mg/g), or high salt (40 mg/g) diets for 5, 10, and 20 days. mRNA levels for the two AT 1 receptor subtypes were determined in adrenal gland, kidney, liver, and lung. In all of the organs examined, with the exception of the adrenal glands, low salt diet led to a transient decrease in the abundance of AT 1A receptor mRNA but not of AT 1B mRNA, which reached their nadirs between days 5 and 10 of feeding. In the adrenal gland, in which the AT 1B receptor is predominant, low salt diet led to a transient increase in the expression of this receptor gene, with a maximum around day 10 of feeding. High salt diet exerted no significant influence on AT 1 receptor gene expression in these organs. These findings indicate that the rate of salt intake, in particular, a reduction of salt intake, significantly influences AT 1 receptor gene expression in an organ-, time-, and subtype-dependent fashion. It appears that AT 1 receptor subtypes are differentially influenced by low salt intake, in that AT 1B receptor gene expression increases and AT 1A receptor gene expression decreases in this situation. This differential response of AT 1 receptor gene expression may be relevant for the organism to be able to adapt to a reduction in oral salt intake.
Schmid et al. (Tue,) reported a other. Low and high salt diets vs. Normal salt (6 mg/g) was evaluated on mRNA levels for the two AT1 receptor subtypes in adrenal gland, kidney, liver, and lung. Low dietary salt intake (0.2 mg/g) transiently decreased AT1A receptor mRNA in most organs but increased AT1B receptor mRNA in the adrenal gland, showing an organ- and subtype-dependent response.