Original Article
Copyright ©2013 Baishideng Publishing Group Co.
World J Hypertens. May 23, 2013; 3(2): 9-17
Published online May 23, 2013. doi: 10.5494/wjh.v3.i2.9
Figure 1
Figure 1 Blood pressures and heart weights of hypertensive hamsters. Time course for changes in noninvasively measured systolic blood pressure in two-kidney, one-clip (2K1C) hypertensive hamsters. Either an angiotensin (Ang) converting enzyme inhibitor (ACE-I), an Ang II type 1 receptor antagonist (ARB), or saline was administered, beginning at 2 wk after renal artery clipping; n = 6-8 for each time point. A: Hamster hearts were removed and weighed at 18 wk after clipping, n = 6 per group; B: Results are presented as means ± SEMs. bP < 0.01, aP < 0.05 vs Vehicle; dP < 0.01 vs Sham.
Figure 2
Figure 2 Chymase and angiotensin converting enzyme mRNA expressions and localization of mast cell in two-kidney, one-clip hamsters. Time course for changes in chymase and angiotensin converting enzyme (ACE) mRNA expression in the heart, aorta, and lung in sham-operated and two-kidney, one-clip (2K1C) hamsters. Chymase mRNA expression in (A) heart, (C) aorta, and (E) lung. ACE mRNA expression in (B) heart, (D) aorta, and (F) lung. Photomicrograph of the same section stained by toluidine blue shows the heart and the ascending aorta from sham-operated (G, I) and 2K1C (H, J) hamster. Mast cells identified by toluidine blue staining (arrowheads) appear in epicardium of the heart (G, H) and adventitia of the aorta (I, J). Results are presented as means ± SEM; n = 5-6 per group. aP < 0.05 vs Sham.
Figure 3
Figure 3 Cardiac tissue angiotensin II-forming activity in two-kidney, one-clip hypertensive hamsters. Cardiac tissue (A) total, (B) chymase-, (C) angiotensin converting enzyme (ACE)-, and (D) other enzyme-dependent Ang II-forming activities in sham-operated and two-kidney, one-clip (2K1C) hypertensive hamsters. Hamster hearts were removed, and activities were measured at 18 wk after clipping either without or with ACE inhibitor (ACE-I) (Temocapril; 30 mg/kg per day) or angiotensin II type 1 receptor antagonist (ARB) (CS866; 10 mg/kg per day) treatment. Results are presented as means ± SEMs; n = 6 per group. bP < 0.01, aP < 0.05, cP < 0.1 vs Vehicle; dP < 0.01 vs Sham.
Figure 4
Figure 4 Aortic tissue angiotensin II-forming activity in two-kidney, one-clip hypertensive hamsters. Aortic tissue (A) total, (B) chymase-, (C) angiotensin (Ang) converting enzyme (ACE)-, and (D) other enzyme-dependent Ang II-forming activities in sham-operated and two-kidney, one-clip (2K1C) hypertensive hamsters. Hamster aortas were removed, and activities were measured at 18 wk after clipping either without or with ACE inhibitor (ACE-I) (Temocapril; 30 mg/kg per day) or angiotensin II type 1 receptor antagonist (ARB) (CS866; 10 mg/kg per day) treatment. Results are presented as means ± SEM’s; n = 6 per group. aP < 0.05; bP < 0.1 vs Vehicle; cP < 0.05 vs Sham.
Figure 5
Figure 5 Pulmonary tissue angiotensin II-forming activity in two-kidney, one-clip hypertensive hamsters. Pulmonary tissue (A) total, (B) chymase-, (C) angiotensin (Ang) converting enzyme (ACE)-, and (D) other enzyme-dependent Ang II-forming activities in sham-operated and two-kidney, one-clip (2K1C) hypertensive hamsters. Hamster lungs were removed, and activities were measured at 18 wk after clipping either without or with ACE inhibitor (ACE-I) (Temocapril; 30 mg/kg per day) or angiotensin II type 1 receptor antagonist (ARB) (CS866; 10 mg/kg per day) treatment. Results are presented as means ± SEMs; n = 6 per group. aP < 0.05, bP < 0.01 vs Vehicle; cP < 0.05 vs Sham.