title: Dietary salt intake modulates angiotensin II type 1 receptor gene expression.
abstract: This study aimed to characterize the influence of dietary salt intake on the gene expression of angiotensin II type 1 (AT1) 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 AT1 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 AT1A receptor mRNA but not of AT1B mRNA, which reached their nadirs between days 5 and 10 of feeding. In the adrenal gland, in which the AT1B 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 AT1 receptor gene expression in these organs. These findings indicate that the rate of salt intake, in particular, a reduction of salt intake, significantly influences AT1 receptor gene expression in an organ-, time-, and subtype-dependent fashion. It appears that AT1 receptor subtypes are differentially influenced by low salt intake, in that AT1B receptor gene expression increases and AT1A receptor gene expression decreases in this situation. This differential response of AT1 receptor gene expression may be relevant for the organism to be able to adapt to a reduction in oral salt intake.
authors.affiliation: Institut für Physiologie, Universität Regensburg, Germany.
authors.forename: C
authors.initials: C
authors.lastname: Schmid
authors.forename: H
authors.initials: H
authors.lastname: Castrop
authors.forename: J
authors.initials: J
authors.lastname: Reitbauer
authors.forename: R
authors.initials: R
authors.lastname: Della Bruna
authors.forename: A
authors.initials: A
authors.lastname: Kurtz
mesh_terms: D000311:Adrenal Glands / Q000187:drug effects / Q000378:metabolism; D000804:Angiotensin II / Q000187:drug effects / Q000235:genetics*; D000818:Animals; D001345:Autoradiography; D017931:DNA Primers; D018076:DNA, Complementary / Q000032:analysis / Q000235:genetics; D003627:Data Interpretation, Statistical; D015870:Gene Expression; D007668:Kidney / Q000187:drug effects / Q000378:metabolism; D008099:Liver / Q000187:drug effects / Q000378:metabolism; D008168:Lung / Q000187:drug effects / Q000378:metabolism; D008297:Male; D016133:Polymerase Chain Reaction; D015347:RNA Probes; D012333:RNA, Messenger / Q000032:analysis / Q000235:genetics; D051381:Rats; D017207:Rats, Sprague-Dawley; D044140:Receptor, Angiotensin, Type 1; D044139:Receptor, Angiotensin, Type 2; D011945:Receptors, Angiotensin / Q000187:drug effects / Q000235:genetics*; D012083:Renin / Q000097:blood; D017673:Sodium Chloride, Dietary / Q000494:pharmacology*
chemical_list: D017931:DNA Primers; D018076:DNA, Complementary; D015347:RNA Probes; D012333:RNA, Messenger; D044140:Receptor, Angiotensin, Type 1; D044139:Receptor, Angiotensin, Type 2; D011945:Receptors, Angiotensin; D017673:Sodium Chloride, Dietary; D000804:Angiotensin II; D012083:Renin