Syzygium gratum Extract Alleviates Vascular Alterations in Hypertensive Rats

Abstract

Background and Objectives: Syzygium gratum (SG) is a local vegetable and widely consumed in Thailand. Previously, a strong antioxidative effect of SG extract has been reported. The effects of SG extract on hypertension have remained unknown. The effect of SG aqueous extract on blood pressure and vascular changes were examined in L-NAME-induced hypertensive rats (LHR), and its potential active constituents were also explored. Materials and Methods: Male Sprague Dawley rats were allocated to control, L-NAME (40 mg/kg/day), L-NAME + SG (100, 300, 500 mg/kg/day), or captopril (5 mg/kg/day) groups. The components of SG extract were analyzed. Results: The analysis of aqueous SG extract was carried out using HPLC-Mass spectroscopy, and phenolic compounds could be identified as predominant components which might be responsible for its antihypertensive effects observed in the LHR model (p < 0.05). Additionally, SG extract also improved vascular responses to acetylcholine and decreased vascular remodeling in LHR (p < 0.05). Enhancements of eNOS expression and plasma nitric oxide metabolite levels, and attenuation of angiotensin converting enzyme (ACE) activity and plasma angiotensin II levels were observed in the LHR group treated with SG. Moreover, SG exhibited strong antioxidant activities by reducing vascular superoxide generation and systemic malondialdehyde in LHRs. Captopril suppressed high blood pressure and alleviated vascular changes and ACE activity in LHRs, similar to those of the SG extract (p < 0.05). Conclusion: Our results suggest that the SG extract exhibited antihypertensive effects, which is relevant to alleviation of vascular dysfunction and vascular remodeling of LHRs. These effects might be mediated by phenolic compounds to inhibit ACE activity and scavenge reactive oxygen species in LHR.

Diosmetin Ameliorates Vascular Dysfunction and Remodeling by Modulation of Nrf2/HO-1 and p-JNK/p-NF-κB Expression in Hypertensive Rats

“…It is well established that captopril is an antihypertensive drug due to its chemical structure, which can inhibit ACE [ 6 , 59 ]. The cascular effects of captopril in the present study were consistent with previous studies [ 40 , 54 ]). Captopril also has indirect-vasorelaxant effects via increasing bradykinin production [ 60 ].…”

“…L-NAME causing systemic hypertension related to decreasing NO bioavailability resulting in vascular dysfunction and hypertension in animals has been noted [ 5 , 40 , 41 ]. This study found that the rats that received L-NAME had high blood pressure and decreased ACh-induced vascular relaxation in isolated aortic and mesenteric preparations.…”

Novel ACE Inhibitory Peptides Derived from Yeast Hydrolysates: Screening, Inhibition Mechanisms and Effects on HUVECs

“…41,42 It was suggested that captopril induced NO production in the hypertension rats by promoting eNOS expression. 44,45 Moreover, ACE inhibitory peptides such as IPP, VPP, MHTDD, and GHTDD increased NO production in HUVECs. 15,35 However, the definite mecha-nisms of NO secretion enhancement have not been fully illustrated.…”

“…Previous studies have revealed that, in addition to acting on the RAS system, ACE inhibitors may also improve endothelial function by inhibiting the production of angiotensin II and reducing bradykinin (BK) degradation, promoting NO production. , Amaranth trypsin-digested glutelins (TDGs) were proven to induce endothelial NO production and consequent vasodilation through their ACE inhibitory activity . ACE inhibitory drugs, such as perindopril and captopril, were found to improve NO secretion. , It was suggested that captopril induced NO production in the hypertension rats by promoting eNOS expression. , Moreover, ACE inhibitory peptides such as IPP, VPP, MHTDD, and GHTDD increased NO production in HUVECs. , However, the definite mechanisms of NO secretion enhancement have not been fully illustrated.…”

Butterfly Pea Flower (Clitoria ternatea Linn.) Extract Ameliorates Cardiovascular Dysfunction and Oxidative Stress in Nitric Oxide-Deficient Hypertensive Rats

“…Several lines of evidence have reported that L-NAME-induced hypertension is related to reduce NO bioavailability, resulting in endothelial dysfunction and hypertension [ 39 , 40 ]. This study demonstrated that hypertensive rats had a reduction in vasorelaxant responses to ACh without changes in their response to a NO donor.…”