Published online before print April 4, 2005, doi: 10.1161/01.HYP.0000161990.98383.ad
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(Hypertension. 2005;45:853.)
© 2005 American Heart Association, Inc.
Original Articles |
High-Salt Diet Inhibits Expression of Angiotensin Type 2 Receptor in Resistance Arteries
From the Laboratory of Molecular and Integrative Physiology, Faculty of Medicine, University Los Andes, Chile.
Correspondence to Luis Michea, MD, PhD, Laboratory of Cellular and Molecular Physiology, Faculty of Medicine, University Los Andes, S. Carlos Apoquindo 2200, Las Condes 6782468, Santiago, Chile. E-mail lmichea{at}uandes.cl
Recent studies suggested that type 2 angiotensin receptor (AT2R) could contribute to regulation of blood pressure and/or vascular remodeling. A key question relates to the effects of potential modulators of vascular AT2R expression. In the present work, we evaluated if high salt intake (70 mmol/L NaCl in drinking water) could modulate rat mesenteric artery AT2R function and expression. Angiotensin II dose-response curves were studied in rat perfused pressurized small-diameter arteries in the presence of losartan (AT1R antagonist). Arteries were precontracted with phenylephrine, yielding 
30% decrease in resting diameter. AT2R activation by angiotensin-induced dose-dependent relaxation of precontracted arteries (60.1±9.1% of phenylephrine-induced contraction, P<0.05). In contrast, AT2R-dependent relaxation was not observed in arteries obtained from rats on high-salt diet. Semi-quantitative reverse-transcription polymerase chain reaction experiments demonstrated reduced amount of AT2R mRNA in arteries of rats on high-salt diet (65.5±7.5% of control levels, P<0.05). Western blot studies demonstrated decreased AT2R in mesenteric artery protein fractions of high-salt diet rats (60.0±18.0 of control levels, P<0.05). In a second set of experiments, adrenalectomy (4 days) blunted AT2R-mediated vasorelaxation and decreased AT2R mRNA (72.0±11.0% of control levels, P<0.05). AT2R abundance in protein fractions of mesenteric arteries of ADX rats was also diminished (64.0±13% of control levels, P<0.05). Both, AT2R mRNA and protein downregulation were prevented by mineralocorticoid replacement therapy. Finally, physiological concentrations of aldosterone caused a dose-dependent increase in AT2R mRNA of small diameter mesenteric artery explants. The results are consistent with aldosterone-mediated upregulation AT2R.
Key Words: mineralocorticoid • sodium • hypertension • vascular remodeling • apoptosis
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