The Role of the Activation of the TRPV1 Receptor and of Nitric Oxide in Changes in Endothelial and Cardiac Function and Biomarker Levels in Hypertensive Rats

Figure 1. Comparison of the levels of nitric oxide (NO) (A), tetrahydrobiopterin (BH4) (B), total antioxidant capacity (TAC) (D), malondialdehyde (MDA) (F), in the sera and cyclic guanosin monophosphate (cGMP) (C), phosphodiesterase-3 (PDE-3) (E) in the ventricular tissue of normotensive (N) and hypertensive (H) rats. Values represent the mean ± standard deviation of n = 6, * p ≤ 0.05, by Student’s t-test.

Figure 2. Effects of the capsaicin (CS) and capsazepine (CZ) on levels of nitric oxide (NO) (A), tetrahydrobiopterin (BH4) (B), total antioxidant capacity (TAC) (C), and malondialdehyde (MDA) (D), in the sera of normotensive (N) and hypertensive (H) rats. Values represent the mean ± standard deviation of n = 6, (*, *1, *2, *3) p ≤ 0.05, by Newman’s post hoc test.

Figure 3. Cardiac mechanical performance (A) and nitric oxide levels in liquid effluent (B) in isolated heart of normotensive and hypertensive rats (withe and black bars respectively) in presence or absence of capsaicin (CS) and capsazepine (CZ) treatments. Values represent the mean ± standard deviation of n = 6, (*, **, +, ++, τ, ττ, τττ, γ, γγ) p ≤ 0.05, by Newman’s post hoc test.

Figure 4. Evaluation of the levels of the following parameters in presence or absence of the different treatments. Tetrahydrobiopterin (BH4) (panel A), dihydrobiopterin (BH2) (panel B), nitric oxide (NO) (panel C), cyclic guanosine monophosphate (cGMP) (panel D), phosphodiesterase-3 (PDE-3) (panel E), in ventricular tissue obtained from normotensive (black bars) and hypertensive (white bars) rats. Values represent the mean ± standard deviation of n = 6, (*, *1, *2, *3) p ≤ 0.05, by Newman’s post hoc test.

Figure 5. Expression of guanosine triphosphate cyclohydrolase 1 (GTPCH-1), endothelial nitric oxide synthase (eNOS), protein kinase B (AKT) in ventricular tissue from normotensive and hypertensive rats (black and white bars respectively) with the different treatments. Panel (A): GTPCH-1 expression in ventricular tissue (n = 3–4 rats/group); a = p < 0.05 vs. Normotensive (N), b = p < 0.05 vs. Hypertensive (H), c = p < 0.05 vs. Hypertensive + Capsaicin (H + CS). Panel (B): eNOS expression in left ventricle (n = 3–4 rats/group); a = p < 0.05 vs. Normotensive (N), b = p < 0.05 vs. Hypertensive (H). Panel (C): AKT expression in left ventricle (n = 3–4 rats/group). a = p < 0.05 vs. Normotensive (N), b = p < 0.05 vs. Hypertensive (H), c = p < 0.05 vs. Hypertensive + Capsaicin (H + CS), d = p < 0.05 vs. Normotensive + Capsaicin (N + CS). z = Representative immunoblot. By Duncan’s post hoc test. Data are presented as means ± SEM.

Figure 6. Expression of TRPV1 in the cardiac tissue from normotensive (N) and hypertensive (H) rats, in the absence and presence of capsaicin (CS), capsazepine (CZ), and capsazepine + capsaicin (CZ + CS). (n = 3–4 rats/group). By Duncan’s post hoc test. Data are presented as means ± SEM. (* p < 0.05 of N and H rats).