Figure 1.
IRW administration lowers BP in SHRs.
(A, B and C) SBP, DBP and MAP (mmHg) values from SHRs left untreated (Untr) or treated with a low dose (3mg/Kg BW) or high dose (15mg/Kg BW) of IRW over period of 18 days. BP values for each time point represent the mean BP recorded over a 24 hr period. (D) Heart rate (bpm) of SHRs in the 3 treatment groups over a period of 18 days. Data represented as mean ± SEM from n=6 animals per treatment group. * and *** indicate P<0.05 and P<0.001 respectively, as compared to the untreated group. ‘ns’ indicates not significant compared to the untreated group.
Figure 2.
IRW treatment restores the circadian rhythms of BP in SHRs.
(A, B and C) SBP, DBP and MAP (mmHg) values from SHRs left untreated or treated with a low dose (3mg/Kg BW) or high dose (15mg/Kg BW) of IRW were recorded during light and dark cycles over a period of 18 days. (D) 2way ANOVA to demonstrate the effects of IRW (low and high dose) on circadian rhythm in MAP. Data represented as mean ± SEM from n=6 animals per treatment group.
Figure 3.
IRW treatment restores the nitric oxide contribution to vasodilatation in mesenteric arteries of SHRs.
(A) IRW at the high dose (15mg/Kg BW) but not at the low dose (3mg/Kg BW) significantly increased maximal vasorelaxation in response to MCh. (B, C and D) Addition of L-NAME (100 µM) prior to MCh treatment attenuated vasorelaxation in the high dose (D) but not in the low dose (C) or the untreated (B) groups. Data represented as mean ± SEM from n=6 animals per treatment group. * indicates P<0.05 compared to the untreated group.
Figure 4.
IRW treatment attenuates plasma Ang II levels through possible ACE inhibitory effects.
(A) Plasma Ang II (pg/mL) levels from untreated and high dose (15mg/Kg BW) IRW treated SHRs are shown. (B) Plasma bradykinin (ng/mL) levels from untreated and high dose (15mg/Kg BW) IRW treated SHRs. Data represented as mean ± SEM from n=6 animals per treatment group. * and ** indicate P<0.05 and P<0.01 respectively, as compared to the untreated group.
Figure 5.
IRW treatment attenuates inflammatory markers in SHRs.
(A and B) Relative changes in plasma IL-6 and MCP-1 levels in untreated and high dose (15mg/Kg BW) IRW treated SHRs. (C and D) ICAM-1 and VCAM-1 expression, normalized to ß actin in mesenteric artery lysates from untreated and high dose (15mg/Kg BW) IRW treated animals. Data represented as mean ± SEM from n= 4-6 animals per treatment group. *, ** and *** indicate P<0.05, P<0.01 and P<0.001 respectively, as compared to the untreated group.
Figure 6.
IRW treatment reduces the inflammatory potential of SHR plasma.
(A and B) Confluent HUVEC monolayers were treated with 10% plasma from untreated or high dose IRW treated SHRs for 4 hours. Cells were lysed and immunoblotted for ICAM-1 and VCAM-1 levels. Data from 3-4 different experiments are summarized as mean ± SEM. A representative set of images are shown. *** indicates P<0.001 as compared to the No plasma group.
Figure 7.
IRW treatment restores eNOS expression in SHR vasculature.
Expression of eNOS, normalized to ß actin in mesenteric artery (A) and aortic (B) lysates from untreated and high dose (15mg/Kg BW) IRW treated animals. Data represented as mean ± SEM from n=6 animals per treatment group. * indicates P<0.05 compared to the untreated group.
Figure 8.
IRW treatment attenuates tissue nitrotyrosine and fibrosis in SHRs.
(A and B) Immunostaining for nitrotyrosine in aortic and kidney sections from untreated and high dose (15mg/Kg BW) IRW treated SHRs. (C and D) Immunostaining for type I collagen in aortic and kidney sections from untreated and high dose (15mg/Kg BW) IRW treated SHRs. Data represented as mean ± SEM from n= 3-4 animals per treatment group. * and *** indicate P<0.05 and P<0.001 respectively, as compared to the untreated group.