Objectives To investigate the effect of telmisartan (telmi) on blood pressure, LV morphology, plasma angiotensin II, expression of preproET-1 and ET-1 in left ventricular hypertrophy (LVH) of SHR.

Methods Twenty Wistar-Kyoto (WKY) and twenty SHR were randomised to WKY + Vehicle (n = 10), SHR + Vehicle (n = 10), SHR + telmi (30mg/kg·d, n = 10), WKY + telmi (n = 10) groups. The systolic blood pressure (SBP) was measured at 0, 4, 8, and 12 weeks of the experiment by tail cuff method. The changes of cardiac function were evaluated by Catheterization. The and plasma angiotensin II(Ang II) levels was measured by RIA. The average cardiomyocite diameter was calculated with the aid of an image analyzer (Image ProPlus 5.0). The mRNA expression of preproET-1, ET-1 were measured by RT-PCR.

Results The SBP of telmisartan groups was significantly lower than Vehicle groups (155.25 ± 7.62 vs 202.43 ± 8.21mmHg, P < 0.01). Telmi group increased the left ventricular + dp/dtmax (56.23 ± 7.02 vs 62.30 ± 5.56, P < 0.05),-dp/dtmax (40.02 ± 5.13 vs 45.89 ± 4.36, P < 0.05). And the LVW/BW in SHR + Vehicle were significantly greater than that in WKY + Vehicle (3.02 ± 0.31 vs 2.42 ± 0.24mg/g, P < 0.01), Compared with SHR + Vehicle, after 12 weeks treatment with telmi, the LVW/BW in SHR + telmi decreased significantly (3.02 ± 0.31 vs 2.68 ± 0.25mg/g, P < 0.01). SHR + Telmi group had lower plasma Ang II than that in SHR + vehicle group (475.25 ± 69.31 vs 782.68 ± 70.25 pg/ml, P < 0.01). The cardiomyocite diameter of SHR + Vehicle was significantly larger than that of WKY + Vehicle (17.11 ± 2.81 vs 13.28 ± 3.25 μm, P < 0.05). Compared with SHR + Vehicle, the cardiomyocite diameter in SHR + telmi decreased significantly (14.81 ± 2.96 vs 17.11 ± 2.81 μm, P < 0.05). The expression of preproET-1 mRNA of SHR + telmi decreased 22.3% compared with SHR + Vehicle (P < 0.01), and the ET-1 level in left ventricular were markedly lower in SHR + telmi than that in SHR + Vehicle (177.44 ± 17.03 vs 220.51 ± 20.21, P < 0.05).

Conclusions Telmisartan could preserve cardiac systolic and diastolic function and inhibit left ventricular hypertrophy partially by decreasing Ang II and ET-1 in SHR.