Takeshi Yoneda, Yasuki Kihara, Hiroyuki Takenaka, Yoko Onozawa, Nobuaki Sarai, Toru Kita
Med Sci Monit 2003; 9(12): BR399-402
Available online: 2003-12-02
Background:The Rho/Rho kinase pathway plays an important role in regulation of vascular smooth muscle cell contraction and is involved in the pathogenesis of hypertension. However, little is known about the role of this pathway in the evolution of salt-sensitive hypertension and vascular remodeling. The aim of this study was to examine whether the age-dependent surge of blood pressure after exposure to a high salt-containing diet, which is well-established for Dahl salt-sensitive rats, is primarily regulated by the level of expression of RhoA in arterial vessels.Material/Methods:We examined Dahl salt-sensitive rats at 3 weeks, 6 weeks, and 9 weeks of age (n=10, each). In each group, animals were switched to being fed a diet containing 8% NaCl from one containing 0.3% NaCl. After 7days, mRNA and protein levels of RhoA from the thoracic aorta were quantified.Results:At the time of examination, increases in systolic blood pressure were significantly different depending on the age at which the high salt diet was initiated. The % increases were 34±3% (3-weeks), 20±2% (6-weeks), and 13±2% (9-weeks). Despite these differing changes in blood pressure, mRNA and protein levels of RhoA in the arteries did not differ among the groups.Conclusions:RhoA expression and activity appear not to be the critical determinant of the surge in hypertension when Dahl salt-sensitive rats are exposed to salt-rich diets. Hence, the age-dependent salt-sensitivity must be mediated by alternative pathways.
Keywords: Animals, Aorta, Thoracic - metabolism, Blood Pressure, Gene Expression, Hypertension - etiology, Hypertension - genetics, Hypertension - physiopathology, RNA, Messenger - genetics, RNA, Messenger - metabolism, Rats, Rats, Inbred Dahl, Sodium Chloride - administration & dosage, Sodium, Dietary - administration & dosage, rhoA GTP-Binding Protein - genetics, rhoA GTP-Binding Protein - metabolism