Ang II-induced contraction is impaired in the aortas of renovascular hypertensive animal model

Figures

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  Figure 1. Systolic blood pressure (SBP, mm Hg) measurements in normotensive (2K) and hypertensive (2K-1C) rats, and ACh-induced relaxation. (A) Each point represents the mean ± s.e.m.of measurements carried out for 6 weeks after induction of renovascular hypertension (2K-1C) or Sham surgery (2K) (n = 4–6). *Difference in relation to 2K (P < 0.05). Student's t-test. (B) Concentration–effect curves were constructed in isolated aorta of 2K (n = 4) and 2K-1C (n = 5) rats pre-contracted with phenylephrine. *Difference in the maximum effect with P < 0.05. Student's t-test. In addition, the results of SBP and concentration–effect responses are expressed as area under the curve (AUC, in arbitrary units).

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  Figure 2. Ang II-induced contraction in endothelium-intact rat aortas. Concentration–effect curves to Ang II were constructed for endothelium-intact (E+) aortas in the (A) absence (control), (B, C) in the presence of AT1 receptor antagonist (losartan, 10 µmol/L), (D, E) AT2 receptor antagonist (PD123319, 1 µmol/L), or (F, G) Mas receptor antagonist (A779, 10 µmol/L) in normotensive (2K) and hypertensive (2K-1C) rat aortas. The results of concentration–effect responses are also represented by the area under the curve (AUC, in arbitrary units). Data represent the mean ± s.e.m . (n = 4–10). *Difference at the maximum effect of losartan vs control (P < 0.05); Student's t-test.

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  Figure 3. Endothelial enzymes contributing to Ang II-induced contractions. Concentration–effect curves to Ang II were constructed in the absence (open circle, open square) or in the presence of the enzyme inhibitors (closed circle, closed square) L-NAME (100 µmol/L) (A, B), apocynin (100 µmol/L) (C, D), or indomethacin (indo,10 µmol/L) (E, F) in endothelium-intact normotensive (2K) and hypertensive (2K-1C) rat aortic rings. The area under the curve (AUC, in arbitrary units) were calculated from the individual concentration–response curve plots. Data represent the mean ± s.e.m. (n = 5–11). *Difference at the maximum effect of L-NAME vs control (P < 0.05) by Student's t-test.

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  Figure 4. eNOS mRNA and NO levels. (A) eNOS mRNA expression levels measured in rat aorta homogenate through by qRT-PCR (ΔΔ Ϲt) and normalized to GAPDH. (B) NO levels measured in plasma from normotensive (2K) and hypertensive (2K-1C) rats. Data represent mean ± s.e.m. (n = 5–6). *Difference between 2K-1C vs 2K rats (P = 0.00030) by Student's t-test.

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  Figure 5. Effect of endothelium removal on Ang II-induced contraction Concentration–effect curves to Ang II were constructed for (A,B) endothelium-intact (E+) or (A,B,C) denuded (E−) normotensive (2K) and hypertensive (2K-1C) rat aortas and are expressed as area under the curve (AUC, in arbitrary units) from individual concentration–response curve plots. Data represent mean ± s.e.m. ( n = 7–11). *Difference at the maximum effect between E+ vs E− or 2K-1C vs 2K (P < 0.05). #Difference at the pD2 between E+ vs E− (P < 0.05) by Student's t-test.

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  Figure 6. Basal AT1 and AT2 receptor expression in the aorta and Ang II plasma levels. (A) AT1 and (B) AT2 receptor expression in normotensive (2K) and hypertensive (2K-1C) rats. (C) ELISA detection of Ang II levels in 2K and 2K-1C rat plasma. Data represent mean ± s.e.m . (n = 5–6). *Difference between 2K-1C vs 2K (P < 0.05) by Student's t-test.

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  Figure 7. KCl-induced contraction in rat aorta. Contractile response was induced by KCl (120 mmol/L) in 2K and 2K-1C rat aortic rings. Data represent the mean ± S.E.M. (n = 7–9). *Difference at the maximum effect between E+ vs E− (P < 0.05). #Difference at the maximum effect between 2K-1C vs 2K (P < 0.05) by two-way ANOVA.

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  Figure 8. Basal phospho-IP3 receptor, IP3 receptor, and MLC expression in rat aorta. (A) phospho-IP3 receptor, (B) IP3 receptor, and (C) MLC expression were quantified in 2K and 2K-1C rat aorta VSMC. Data represent the mean ± s.e.m. (n = 4). *Difference between 2K-1C vs 2K (P < 0.05) by Student's t-test.