Angiotensin II Disrupts Axo-Axonal Interaction-Mediated Vasorelaxation in Basilar Arteries of Normotensive and Hypertensive Rats

Figures

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  Figure 1. Representative tracings of nicotine- (50 uM) and TNS- (8 Hz) induced relaxation in endothelium-denuded basilar arterial rings from 20-week-old WKYs and SHRs. (A) Absence of vasorelaxation in SHRs, with summarized data in (B), p-values = 0.002. (C) Concentration-dependent relaxation to norepinephrine (NE, 0.1–1 uM) following U-46619 (0.1 uM) pre-contraction. NE-induced relaxation was significantly attenuated in SHRs. Data mean ± SD; n = number of experiments. (* p < 0.05) vs. WKYs (Student’s t-test).

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  Figure 2. Representative tracing showing that the recovery of nicotine (50 μM)- and TNS (8 Hz)-induced endothelium-denuded relaxation of the basilar arterial ring in SHRs was significantly enhanced by pre-incubation with losartan (1 μM) for 15 min (A). These results are summarized in (B). Nicotine (50 μM)-, TNS-, and isoproterenol-induced vasodilation in the BA was significantly enhanced by oral losartan (10 mg/day) for 30 days (C,D). Values are mean ± SD. n = number of experiments. * p < 0.05 vs. Control. Asterisks indicate a significant difference in the t-test (* p < 0.05) vs. the control group in (B,C). Asterisks indicate a significant difference in Bonferroni post-tests following ANOVA (* p < 0.05) vs. SHR in (D).

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  Figure 3. (A) Nicotine (50 μM)-induced relaxation of the endothelium-denuded basilar arterial rings of WKYs (15 weeks old) was inhibited by pre-treatment with AII (10–100 nM) in a concentration-dependent manner. (B) Isoproterenol (n = 5)-induced relaxation of the BA was significantly inhibited by AII (100 nM). The inhibition of AII was not recovered after AII washout. Values are mean ± SD. n = number of experiments. * p < 0.05 vs. Control. Asterisk indicates a significant difference in Bonferroni post-tests following ANOVA (* p < 0.05) vs. Control group.

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  Figure 4. (A) Nicotine (50 μM)- and TNS (8 Hz)-induced relaxation was inhibited by pre-treatment with AII (100 nM), but this was significantly recovered by marimastat (1 μM). (B) Nicotine (50 μM)- and TNS (8 Hz)-induced relaxation was inhibited by pre-treatment with AII (100 nM), which was significantly recovered by catalase (100 U/mL). (C) The inhibition of AII (100 nM) was also recovered by ferrostatin-1 (10 μM). Values are mean ± SD. n = number of experiments. * p < 0.05 vs. Control. Asterisk indicates a significant difference in Bonferroni post-tests following ANOVA (* p < 0.05) vs. Control group.