astaxanthine and Hypertension

Inflammation plays a key role and is one of the early steps in the pathogenesis of endothelial function, thereby increasing the risk of hypertension (HTN), coronary artery disease (CAD), stroke and several other risk factors of cardiovascular disease (CVD). We assessed the efficacy for improving cardiovascular health (blood pressure, inflammation and endothelial reactivity) over a 4-week intervention period in healthy individuals.. We performed a randomized, double-blinded, placebo-controlled, randomized clinical trial to investigate Curcumin, Eicosapentaenoic acid (EPA), Astaxanthin and Gamma -linoleic acid (GLA) (CEAG) supplements with 80 individuals (30 men and 50 women). The mean age of participants was 48.8 ± 16.0 years. Participants were enrolled and randomized to active or placebo and followed for 4 weeks. Paired and Independent T-tests were used to analyze the mean differences between and within groups.. The primary endpoints of the study were the effect on inflammatory markers (IL-6, CRP), endothelial function and blood pressure at 4 weeks. There was a significant reduction in mean SBP at 4 weeks in the CEAG group compared to placebo [mean ± SD 4.7 ± 6.8 (p = 0.002)]. Relative to placebo, active group showed a significant decrease in High sensitivity C Reactive Protein (hsCRP) (-0.49 ± 1.9 vs + 0.51 ± 2.5, p = 0.059) and blunted increase in IL-6 (+0.2 vs + 0.4 in placebo, p = 0.60).. Inflammatory markers were reduced or blunted by CEAG, with a robust increase in both EPA levels and the fatty acid index. Furthermore, systolic BP was reduced over 4 weeks with concurrent improvement in endothelial function. CLINICALTRIALS.. NCT03906825.

Topics: Adolescent; Adult; Aged; Biomarkers; Blood Pressure; C-Reactive Protein; Cardiovascular Diseases; Coronary Artery Disease; Dietary Supplements; Double-Blind Method; Eicosapentaenoic Acid; Endothelium; Fatty Acids, Omega-3; Female; gamma-Linolenic Acid; Healthy Volunteers; Humans; Hypertension; Interleukin-6; Male; Middle Aged; Xanthophylls; Young Adult

Hypertension is a major global health problem. It is a major risk factor of cardiovascular disease. One of the most used experimental models in studying antihypertensive action is the deoxycorticosterone acetate (DOCA)-salt hypertensive rat. This study aimed to investigate the cardiovascular protective effect of astaxanthin (ASX) in DOCA-salt-induced hypertension and its possible underlying mechanisms.. A total of 48 adult male Wistar albino rats were divided into three groups: control, DOCA, and DOCA + ASX. Blood pressure, serum cardiac enzyme levels, some oxidative stress and inflammatory biomarker levels, and lipid profile levels were measured. The weight of the left ventricle to tibial length ratio was calculated. Apoptosis detection and total genomic DNA extraction in aortic and cardiac tissues were investigated. The apoptotic marker BAX was also immunohistochemically assessed in the heart and aorta.. Compared to the control group, the DOCA group was associated with a significant increase in blood pressure, serum cardiac enzyme levels, oxidative stress and inflammatory biomarker levels, lipid profile except serum high-density lipoprotein (HDL), weight of the left ventricle to tibial length, and total released DNA fragmentation level of the left ventricle and aorta and a significant decrease in reduced glutathione (GSH) and HDL. Compared to the DOCA group, the DOCA + ASX group significantly improved the DOCA-induced changes.. ASX has beneficial protective effects on DOCA-salt-induced hypertension via DNA fragmentation protection, apoptosis inhibition, antioxidant, anti-inflammatory, and its effects on lipid levels.

Topics: Acetates; Animals; Blood Pressure; Desoxycorticosterone Acetate; Hypertension; Lipids; Male; Rats; Rats, Wistar

Oxidative stress, the renin-angiotensin system (RAS), and inflammation are some of the mechanisms involved in the pathogenesis of hypertension. The aim of this study is to examine the protective effect of the chronic administration of astaxanthin, which is extracted from the shell of crabs and shrimps, into hypothalamic paraventricular nucleus (PVN) in spontaneously hypertensive rats. Animals were randomly assigned to 2 groups and treated with bilateral PVN infusion of astaxanthin or vehicle (artificial cerebrospinal fluid) through osmotic minipumps (Alzet Osmotic Pumps, Model 2004, 0.25 μL/h) for 4 weeks. Spontaneously hypertensive rats had higher mean arterial pressure and plasma level of norepinephrine and proinflammatory cytokine; higher PVN levels of reactive oxygen species, NOX2, NOX4, IL-1β, IL-6, ACE, and AT1-R; and lower PVN levels of IL-10 and Cu/Zn SOD, Mn SOD, ACE2, and Mas receptors than Wistar-Kyoto rats. Our data showed that chronic administration of astaxanthin into PVN attenuated the overexpression of reactive oxygen species, NOX2, NOX4, inflammatory cytokines, and components of RAS within the PVN and suppressed hypertension. The present results revealed that astaxanthin played a role in the brain. Our findings demonstrated that astaxanthin had protective effect on hypertension by improving the balance between inflammatory cytokines and components of RAS.

Topics: Animals; Anti-Inflammatory Agents; Antihypertensive Agents; Arterial Pressure; Cytokines; Disease Models, Animal; Hypertension; Inflammation Mediators; Infusions, Parenteral; Male; Paraventricular Hypothalamic Nucleus; Rats, Inbred SHR; Rats, Inbred WKY; Renin-Angiotensin System; Time Factors; Xanthophylls

The aim of this study was to investigate the effects of egg yolk powder enriched with astaxanthin (ASX-E) on blood pressure in spontaneously hypertensive rats (SHR) and to verify the benefits of ASX-E as a functional food. To investigate the antihypertensive effect, SHR were fed with an ASX-E mixed diet before hypertension development. Blood pressures were determined periodically during the study by the tail-cuff method. At the end of the study, animals were euthanized, and their thoracic aortas were collected to determine vascular conductance. The thoracic aorta tension was measured with a force displacement transducer. Concentration-dependent response relationships were determined by cumulative addition of 10

Topics: Animals; Antihypertensive Agents; Aorta, Thoracic; Blood Pressure; Diet; Dietary Supplements; Endothelium, Vascular; Hypertension; Male; Rats; Rats, Inbred SHR; Vasoconstriction; Vasodilation; Vasodilator Agents; Xanthophylls

Oxidative stress aggravates mitochondrial injuries and accelerates the proliferation of vascular smooth muscle cells (VSMCs), which are important mechanisms contributing to vascular remodeling in hypertension. We put forward the hypothesis that Astaxanthin (ATX), known to possess strong features of antioxidant, could attenuate vascular remodeling by inhibiting VSMC proliferation and improving mitochondrial function. The potential effects of ATX were tested on spontaneously hypertensive rats (SHRs) and cultured VSMCs that injured by angiotensin II (Ang II). The results showed that ATX lowered blood pressure, reduced aortic wall thickness and fibrosis, and decreased the level of reactive oxygen species (ROS) and H

Topics: Animals; Fibrinolytic Agents; Hypertension; Male; Mitochondria; Muscle, Smooth, Vascular; Oxidative Stress; Rats; Rats, Inbred WKY; Vascular Remodeling; Xanthophylls

The aim of this study was to investigate the effects of astaxanthin-enriched diet on blood pressure, cardiac hypertrophy, both vascular structure and function and superoxide ((*)O(2-)) production in spontaneously hypertensive rats (SHR). Twelve-week-old SHR were treated for 8 weeks with an astaxanthin-enriched diet (75 or 200mg/kg body weight per day). Systolic blood pressure was monitorized periodically during the study by the tail cuff method. At the end of the study animals were sacrificed and heart, kidneys and aorta were removed. Left ventricular weight/body weight ratio was used as left ventricular hypertrophy index (LVH). Vascular function and structure were studied in conductance (aortic rings) and resistance (renal vascular bed) arteries. Also (*)O(2-) production was evaluated by lucigenin-enhanced chemiluminescence. Systolic blood pressure was lower in astaxanthin-treated groups than the control group from the first week of treatment, and LVH was significantly reduced. Astaxanthin improved endothelial function on resistance arteries, but had no effect on aorta. These effects were accompanied by a decrease in oxidative stress and improvements in NO bioavailability. Taken together, these results show that diet supplemented with astaxanthin has beneficial effects on hypertension, by decreasing blood pressure values, improving cardiovascular remodeling and oxidative stress.

Topics: Animals; Antihypertensive Agents; Aorta; Blood Pressure; Diet; Disease Models, Animal; Dose-Response Relationship, Drug; Endothelium, Vascular; Hypertension; Hypertrophy, Left Ventricular; Male; NADPH Oxidases; Nitric Oxide; Oxidative Stress; Rats; Rats, Inbred SHR; Renal Artery; Superoxides; Time Factors; Vascular Resistance; Vasodilation; Vasodilator Agents; Xanthophylls

It is known that vitamin E and some carotenoids have antioxidant activities that alleviate endothelial dysfunction and play a protective role against cardiovascular disease. The current study was designed to examine the hypothesis that astaxanthin, a red pigment carotenoid found in salmonid and crustacean aquaculture, protects stroke-prone spontaneously hypertensive rats (SHRSP) from vascular oxidative damage, hypertension, and cerebral thrombosis. Male 6-week-old SHRSP were classified into 4 groups: a control group, 2 astaxanthin groups, and a vitamin E group. The treated animals were given either astaxanthin or vitamin E for 3 weeks. Body weights in each group were not significantly different from control group during the treatment period, but the usual increase in systolic blood pressure in SHRSP observed with age was significantly suppressed by treatment. Thrombogenesis, assessed using a helium-neon (He-Ne) laser technique in pial blood vessels, together with antioxidant activity, assessed by measuring urinary 8-OHdG levels, were significantly moderated. Urinary nitric oxide (NO) metabolites were increased after treatment. These results supported our hypothesis and strongly suggested that the antithrombotic and antihypertensive effects of astaxanthin or vitamin E may be related to an increase in bioavailable NO, possibly mediated by decreased inactivation of NO by reactive oxygen species.

Topics: 8-Hydroxy-2'-Deoxyguanosine; Animals; Antihypertensive Agents; Antioxidants; Cardiovascular Diseases; Deoxyguanosine; Dose-Response Relationship, Drug; Fibrinolytic Agents; Hypertension; Intracranial Thrombosis; Male; Nitrates; Nitric Oxide; Nitrites; Oxidative Stress; Rats; Rats, Inbred SHR; Risk Factors; Specific Pathogen-Free Organisms; Stroke; Xanthophylls

Glucose and lipid metabolic parameters play crucial roles in metabolic syndrome and its major feature of insulin resistance. This study was designed to investigate whether dietary astaxanthin oil (ASX-O) has potential effects on metabolic syndrome features in an SHR/NDmcr-cp (cp/cp) rat model. Oral administration of ASX (50 mg/kg/day) for 22 weeks induced a significant reduction in arterial blood pressure in SHRcp. It also significantly reduced the fasting blood glucose level, homeostasis index of insulin resistance (HOMA-IR), and improved insulin sensitivity. The results also showed an improved adiponectin level, a significant increase in high-density lipoprotein cholesterol, a significant decrease in plasma levels of triglycerides, and non-esterified fatty acids. Additionally, ASX showed significant effects on the white adipose tissue by decreasing the size of the fat cells. These results suggest that ASX ameliorates insulin resistance by mechanisms involving the increase of glucose uptake, and by modulating the level of circulating lipid metabolites and adiponectin.

Topics: Adiponectin; Adipose Tissue; Administration, Oral; Animals; Blood Cell Count; Blood Glucose; Blood Pressure; Body Weight; Cell Size; Heart Rate; Hypertension; Insulin; Insulin Resistance; Lipid Metabolism; Male; Metabolic Syndrome; Rats; Rats, Inbred SHR; Rats, Wistar; Xanthophylls

We investigated the effects of a dietary astaxanthin (ASX-O) on oxidative parameters in spontaneously hypertensive rats (SHR), by determination of the level of nitric oxide (NO) end products nitrite/nitrate (NO2-/NO3-) and lipid peroxidation in ASX-O-treated SHR. Oral administration of the ASX-O significantly reduced the plasma level of NO2-/NO3- compared to the control vehicle (p<0.05). The lipid peroxidation level, however, was reduced in both ASX-O- and olive oil-treated groups. We also analyzed the post-treatment effects of ASX-O on the vascular tissues by examining the changes in the aorta and coronary arteries and arterioles. The dietary ASX-O showed significant reduction in the elastin bands in the rat aorta (p<0.05). It also significantly decreased the [wall : lumen] aerial ratio of the coronary arteries. These results suggest that ASX-O can modulate the oxidative condition and may improve vascular elastin and arterial wall thickness in hypertension.

Topics: Animals; Antihypertensive Agents; Antioxidants; Aorta, Thoracic; Blood Pressure; Coronary Vessels; Elastin; Heart; Heart Rate; Hypertension; Lipid Peroxidation; Male; Muscle, Smooth, Vascular; Myocardium; Nitric Oxide; Rats; Rats, Inbred SHR; Xanthophylls

Astaxanthin is a natural antioxidant carotenoid that occurs in a wide variety of living organisms. We investigated, for the first time, antihypertensive effects of astaxanthin (ASX-O) in spontaneously hypertensive rats (SHR). Oral administration of ASX-O for 14 d induced a significant reduction in the arterial blood pressure (BP) in SHR but not in normotensive Wistar Kyoto (WKY) strain. The long-term administration of ASX-O (50 mg/kg) for 5 weeks in stroke prone SHR (SHR-SP) induced a significant reduction in the BP. It also delayed the incidence of stroke in the SHR-SP. To investigate the action mechanism of ASX-O, the effects on PGF(2alpha)-induced contractions of rat aorta treated with NG-nitro-L-arginine methyl ester (L-NAME) were studied in vitro. ASX-O (1 to 10 microM) induced vasorelaxation mediated by nitric oxide (NO). The results suggest that the antihypertensive effect of ASX-O may be due to a NO-related mechanism. ASX-O also showed significant neuroprotective effects in ischemic mice, presumably due to its antioxidant potential. Pretreatment of the mice with ASX-O significantly shortened the latency of escaping onto the platform in the Morris water maze learning performance test. In conclusion, these results indicate that astaxanthin can exert beneficial effects in protection against hypertension and stroke and in improving memory in vascular dementia.

Topics: Animals; Antihypertensive Agents; Aorta, Abdominal; beta Carotene; Blood Pressure; Hypertension; In Vitro Techniques; Male; Neuroprotective Agents; Rats; Rats, Inbred SHR; Rats, Inbred WKY; Rats, Wistar; Stroke; Vasodilation; Xanthophylls

The current study was designed to determine the effects of a dietary astaxanthin (ASX-O) on vascular reactivity in spontaneously hypertensive rats (SHR), in order to verify its antihypertensive action mechanism. We evaluated contractions induced by phenylephrine (Phe), angiotensin II (Ang II) and the xanthine/xanthine oxidase (Xan/XOD) system, and relaxations induced by sodium nitroprusside (SNP) as well as endothelium-dependent relaxations mediated by acetylcholine (ACh) in thoracic aorta of the SHR, with and without ASX-O intervention. We also investigated the effects of ASX-O on blood rheology using a microchannel array system. In this study, ASX-O showed a significant modulatory effect on nitric oxide (NO)-induced vasorelaxation by the NO-donor SNP (p<0.05). However, it did not show significant effects in restoring the impaired endothelium-dependent relaxation to ACh in the SHR. On the other hand, the constrictive effects by Phe, Ang II and Xan/XOD were ameliorated by ASX-O (p<0.05). ASX-O also demonstrated significant hemorheological effect by decreasing the microchannel transit time of whole blood. In conclusion, the results suggest that ASX-O may act in modulating the blood fluidity in hypertension, and that the antihypertensive effects of ASX-O may be exerted through mechanisms including normalization of the sensitivity of the adrenoceptor sympathetic pathway, particularly [alpha]-adrenoceptors, and by restoration of the vascular tone through attenuation of the Ang II- and reactive oxygen species (ROS)-induced vasoconstriction.

Topics: Animals; Antihypertensive Agents; Aorta; beta Carotene; Hemorheology; Hypertension; In Vitro Techniques; Male; Rats; Rats, Inbred SHR; Vasoconstriction; Vasodilation; Xanthophylls