Key result
Losartan and captopril reduced systolic blood pressure by ~40 mm Hg, but only long-term losartan treatment significantly changed VSMC phenotype and proliferative status.
Why the study?
Does chronic losartan or captopril treatment alter vascular smooth muscle cell phenotype and vascular function in spontaneously hypertensive rats?
Does chronic losartan or captopril treatment alter vascular smooth muscle cell phenotype and vascular function in spontaneously hypertensive rats?
Long-term losartan treatment alters vascular smooth muscle cell phenotype and proliferative status independent of blood pressure lowering, an effect not observed with captopril.
May support vascular effects of RAS inhibitors in hypertensive rats; leaves open human translation.
The aim of this study was to investigate the effect of chronic losartan or captopril on vascular smooth muscle cell (VSMC) phenotype and vascular function in spontaneously hypertensive rats. Male 12-week-old rats were treated for 16 weeks with losartan (15 mg/kg per day) or captopril (60 mg/kg per day) in their drinking water. Systolic blood pressure, measured by the tail-cuff method, was reduced approximately 40 mm Hg in both treatment groups compared with a nontreated control group. Cell structure and proliferation studies were performed in VSMCs obtained from rat carotid arteries. Cells from the losartan-treated group showed a significant reduction in size, total protein content, and nucleus number, as well as proliferation after stimulation with 10% fetal calf serum and an increased percentage of cells in the G(1) phase compared with the control and captopril-treated groups. Functional studies were performed in isolated carotid arteries from these groups. Contractions elicited by 75 mmol/L KCl or 10(-)(7) mol/L norepinephrine and relaxations elicited by acetylcholine were similar in all groups. Concentration-response curves to angiotensin I or angiotensin II (10(-)(10) to 3x10(-)(7) mol/L) were almost abolished in the losartan-treated group and were not modified by preincubation with the angiotensin type 2 receptor antagonist PD 123,319. These results suggest that long-term losartan treatment significantly changes VSMC phenotype and proliferative status, apparently unrelated to blood pressure lowering or to endothelial function improvements.
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Bravo et al. (2001) studied Spontaneously hypertensive rats. Losartan or captopril vs. Nontreated control group was evaluated on Vascular smooth muscle cell (VSMC) phenotype and vascular function. Losartan and captopril reduced systolic blood pressure by ~40 mm Hg, but only long-term losartan treatment significantly changed VSMC phenotype and proliferative status.
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