Dietary carotenoids to improve hypertension

Abstract

Hypertension is one of the major risk factors for cardiovascular diseases and the main reason for premature death in older adults. Although antihypertensive medications have been used frequently, hypertension prevalence has increased in the last decade. Lifestyle improvement is a cornerstone of hypertension prevention and control. High dietary consumptions of fruits and vegetables are linked to reduced risks of high blood pressure. Carotenoids are natural tetraterpene pigments produced by bacteria, fungi, algae, some animals, and various plants. Because of their high pharmacological potential and safety, they have been mentioned as unique therapeutic agents for a diverse range of diseases. Carotenoids modulate high blood pressure. They also have several additional benefits for the cardiovascular system, including antioxidative, anti-inflammatory, anti-atherogenic, and antiplatelet effects. They improve endothelial function and metabolic profile, as well. In the present article, we reviewed the literature data regarding carotenoids' influence on hypertension in both preclinical and clinical studies. Furthermore, we reviewed the underlying mechanisms associated with antihypertensive properties derived from in vitro and in vivo studies. Suppressing reactive oxygen species (ROS) production, Inhibiting angiotensin-II, endothelin-1, and oxidized low-density lipoprotein; and also nitric oxide enhancement are some of the mechanisms by which they lower blood pressure. The present article indicated that astaxanthine, β-carotene, bixin, capsanthin, lutein, crocin, and lycopene have antihypertensive properties. Having significant antioxidant properties, they can decrease high blood pressure and concomitant comorbidities.

Keywords: Blood pressure; Carotenoids; Hypertension; Vasodilation.

Graphical abstract

Fig. 1

Chemical structures of carotenoids.

Fig. 2

A schematic illustration of antihypertensive mechanisms of carotenoids. Carotenoids by inhibition of ROS, angiotensin II, and NF-κB induce antihypertensive effects. → present the promote/activate and ⊥ present the inhibitory/suppressive effects. CAT: catalase, eNOS: endothelial nitric oxide synthase, GR: glutathione reductase, GSH-Px: glutathione peroxidase, HO-1: heme oxygenase-1, L-arg: l-arginine, LOX-1: lectin-like ox-LDL receptor 1, NADPH oxidase: nicotinamide adenine dinucleotide phosphate oxid, NF-κB: nuclear factor-κB, NO: nitric oxide, Nrf2: nuclear factor-erythroid 2-like 2, ox-LDL: oxidized low-density lipoprotein, ROS: reactive oxygen species, SOD: superoxide dismutase.

Fig. 3

A schematic illustration of antihypertensive mechanisms of carotenoids. Carotenoids by inhibition of inflammation (TNF-α, LOX-1, NF-κB, VCAM, ICAM, and MCP-1), endothelin-1 receptor, activation of KCa3.1 potassium channels, and intensifying NO production induce antihypertensive effects. → present the promote/activate and ⊥ present the inhibitory/suppressive effects. Akt: protein kinase B, eNOS: endothelial nitric oxide synthase, ERK: extracellular signal-regulated kinase, ET-1: endothelin-1 receptor, ICAM: intercellular adhesion molecule, L-arg: l-arginine, LOX-1: lectin-like ox-LDL receptor 1, NO: nitric oxide, MCP-1: monocyte chemoattractant protein-1, ox-LDL: oxidized low-density lipoprotein, TNF-α: tumor necrosis factor-α, VCAM: vascular cell adhesion molecule.