Table 1.

Mechanisms of action of garlic and its constituents in lowering blood pressure.

Biological Factors	Physiologic Effect	Action of Garlic and Its Components
Oxidative stress	Oxidative stress can lead to endothelial dysfunction and the inability to promote vasodilation, fibrinolysis, and anti-aggregation [49].	SAC can trap ROS and lower the activity of NADPH oxidase. AG increases the activity of superoxide dismutase. Allicin scavenges free radicals and traps OH. Both SAC and Allicin reduce Angiotensin II-induced ROS formation [5].
NF-κB	NF-κB can activate genes that produce pro-inflammatory cytokines like tumor necrosis factor-alpha (TNF-α) and interleukin-1 (IL-1). These cytokines can cause inflammation in the blood vessels, which contributes to endothelial dysfunction [50].	Pyrrolidine dithiocarbamate and SAC suppress NF-κB, which is elevated, along with ROS, in SHRs [5].
H2S	H2S was shown to induce vasodilation and reduce blood pressure [51].	Garlic enhances H2S production by the catalytic effect of CSE [5]. Garlic-derived polysulfides stimulate H2S and enhance NO regulation [6,30].
NO	NO is a potent vasodilator and regulator of vascular tone. It helps to maintain low arterial pressure, inhibit platelet aggregation, and prevent smooth muscle cell proliferation [52].	Garlic increases NO bioavailability and reduces the generation of ROS, such as O2−, which tends to consume NO [5,32,33]. Garlic supplementation can block L-NAME-induced hypertension by promoting NO synthesis [34].
RAAS	The RAAS regulates blood pressure and fluid balance. An overactive RAAS leads to hypertension [53].	SAC and captopril synergistically inhibit ACE in guinea pigs and decrease blood pressure in rats [38]. Garlic and allicin inhibit epithelial Na channels, which leads to less sodium and water retention and a higher urine sodium concentration [5].
VSMCs	VSMCs regulate vascular tone and blood pressure. Changes in the function or phenotype of VSMCs can contribute to the development of hypertension [32].	Garlic, AMS, and DAS interrupt the G0/G1 cell cycle phase and reduce EFK phosphorylation, which leads to decreased VSMC proliferation [5,41,42]. In addition, opening KATP channels by H2S and exogenous H2S donors induces systemic vasodilation [4].