J Asian Nat Prod Res. The effects of ginsenoside Rb 1 on endothelial damage and ghrelin expression induced by hyperhomocysteine. J Vasc Surg. Endothelium-derived relaxing and contracting factors. Ignarro LJ. Biological actions and properties of endothelium- derived nitric oxide formed and released from artery and vein. Circ Res. Nitric oxide: physiology, pathophysiology, and pharmacology. Pharmacol Rev.

Signaling pathway of ginsenoside-Rg1 leading to nitric oxide production in endothelial cells. Relaxation of canine corporal smooth muscle relaxation by ginsenoside saponin Rg 3 is independent from eNOS activation.

Effects of Korean red ginseng Panax ginseng C. Mayer and its isolated ginsenosides and polysaccharides on arterial stiffness in healthy individuals. Am J Hypertens. Vascular smooth muscle dysfunction and remodeling induced by ginsenoside Rg 3 , a bioactive component of ginseng. Toxicol Sci. Ginsenoside Rb 3 inhibits angiotensin II-induced vascular smooth muscle cells proliferation. Basic Clin Pharmacol Toxicol. Effect of Korean red ginseng on arterial stiffness in subjects with hypertension.

J Altern Complement Med. Tamura Y. Effects of Korean red ginseng on eicosanoid biosynthesis in platelets and vascular smooth muscle cells. Study of various rhubarbs regarding the cathartic effect and endotoxin-induced disseminated intravascular coagulation. Antithrombotic and antiplatelet activities of Korean red ginseng extract. J Pharm Pharmacol.

The protective effects of ginsenosides on human erythrocytes against hemin-induced hemolysis. J Sep Sci.

Improving effect of post-treatment with Panax notoginseng saponins on lipopolysaccharide-induced microcirculatory disturbance in rat mesentery. Clin Hemorheol Microcirc. Antiplatelet and anticoagulant effects of Panax notoginseng: comparison of raw and steamed Panax notoginseng with Panax ginseng and Panax quinquefolium. Platelet antiaggregating activity of ginsenosides isolated from processed ginseng.

Inhibitory activity of ginsenosides isolated from processed ginseng on platelet aggregation. Interaction between warfarin and Korean red ginseng in patients with cardiac valve replacement. Int J Cardiol.

Red ginseng extract improves coronary flow reserve and increases absolute numbers of various circulating angiogenic cells in patients with first ST-segment elevation acute myocardial infarction. Activation of the nuclear receptor LXR by oxysterols defines a new hormone response pathway. J Biol Chem. Weight gain reduction in mice fed Panax ginseng saponin, a pancreatic lipase inhibitor. Bifidus fermentation increases hypolipidemic and hypoglycemic effects of red ginseng.

J Microbiol Biotechnol. Korean red ginseng attenuates hypercholesterolemia- enhanced platelet aggregation through suppression of diacylglycerol liberation in high-cholesterol-diet-fed rabbits. Panax notoginseng saponins attenuate atherosclerosis in rats by regulating the blood lipid profile and an anti-inflammatory action.

Clin Exp Pharmacol Physiol. Total panax notoginsenosides prevent atherosclerosis in apolipoprotein E-knockout mice: role of downregulation of CD40 and MMP-9 expression. Panax notoginseng saponins decrease cholesterol ester via upregulating ATP-binding cassette transporter A1 in foam cells. Anti-hyperlipidemic effects of red ginseng acidic polysaccharide from Korean red ginseng. Panax notoginseng saponins attenuate atherogenesis accelerated by zymosan in rabbits.

Hypolipidemic and antioxidant activities of sanchi radix notoginseng in rats fed with a high fat diet. Ginsenoside-Rd, a purified component from Panax notoginseng saponins, prevents atherosclerosis in apoE knockout mice.

Bolli R. Superoxide dismutase 10 years later: a drug in search of a use. Beneficial actions of superoxide dismutase and catalase in stunned myocardium of dogs. Am J Physiol. Direct measurement of free radical generation following reperfusion of ischemic myocardium.

Role of endothelium-derived nitric oxide in the modulation of canine myocardial mitochondrial respiration in vitro. Implications for the development of heart failure. Dichloroacetate improves cardiac efficiency after ischemia independent of changes in mitochondrial proton leak.

Protective effect of Korean Panax ginseng against chromium VI toxicity and free radicals generation in rats. Chang HM. Advances in Chinese medicinal materials research.

World Scientific; Philadelphia: Ginsenosides protect pulmonary vascular endothelium against free radical-induced injury. Free radical scavenging activity of red ginseng aqueous extracts. Protective effect of ginsenosides Rg 2 and Rh 1 on oxidation-induced impairment of erythrocyte membrane properties. Regulation on energy metabolism and protection on mitochondria of Panax ginseng polysaccharide.

An essential role of Nrf2 in American ginseng-mediated anti-oxidative actions in cardiomyocytes. Fu Y, Ji LL. Chronic ginseng consumption attenuates age-associated oxidative stress in rats. Chen X. Cardiovascular protection by ginsenosides and their nitric oxide releasing action.

Ginsenoside Rb 1 blocks homocysteine-induced endothelial dysfunction in porcine coronary arteries. Molecular mechanisms of HIV protease inhibitor-induced endothelial dysfunction. J Acquir Immune Defic Syndr. Antioxidant effects of ginsenoside Re in cardiomyocytes. Anti-lipid peroxilative effect of ginsenoside Rb 1 and Rg 1.

Chin Med J Engl ; — Protection of ischemic hippocampal neurons by ginsenoside Rb 1 , a main ingredient of ginseng root. Neurosci Res. Neuroprotective effect of 20 S -ginsenoside Rg 3 on cerebral ischemia in rats. Neurosci Lett. Ginseng compounds: an update on their molecular mechanisms and medical applications. Curr Vasc Pharmacol. Articles from Journal of Ginseng Research are provided here courtesy of Elsevier. Support Center Support Center.

External link. Please review our privacy policy. The current treatments for IDH include stopping ultrafiltration, increasing dialysate sodium and glucose concentrations, and administration of hypertonic solutions and vasoconstrictor agents [ 1 , 6 , 12 — 14 ]. In the current study, we found that taking 3.

KRG had no significant effects on the baseline blood pressure, suggesting that its beneficial effect is through restoring the vasoconstrictive response to acute plasma changes during hemodialysis.

Furthermore, KRG has been used in different pathologic conditions [ 15 ], and its safety profile has been well studied in patients with normal renal function [ 16 ]. Our results confirmed the safety of using oral form KRG during hemodialysis. Although KRG has been reported to increase blood pressure in non-dialysis patients [ 17 — 19 , 26 , 27 ], we did not observe exacerbation of preexisting hypertension in our patients group A.

The effects of Panax ginseng on regulating blood pressure were controversial due to its complexity of major components and different actions in various pathological conditions [ 18 , 19 , 22 , 28 , 29 ].

It has been reported that dammarenetriol glycosides in Panax ginseng have strong CNS excitatory actions that may cause hypertension, while dammarenediol glycosides in Panax ginseng have sedative and antihypertensive effects [ 26 ]. Three decades ago, Siegel proposed that low-dose Panax ginseng could cause hypertension [ 18 ]. However, high-dose Panax ginseng was shown to increase NO production in recent clinical trials and laboratory experiments [ 29 ], which may reduce blood pressure [ 28 , 30 ].

Furthermore, Panax ginseng induced different responses in different blood vessels taken from rabbits, dogs and humans qualitatively and quantitatively [ 31 ].

Our data suggest that low-dose KRG 3. The mechanism of IDH has been partly attributed to endothelial dysfunction in response to hemodynamic instability, with increased NO and decreased ET-1 during hemodialysis [ 4 , 32 — 34 ].

ET-1 is the most potent vasoconstrictor that is locally produced from vascular endothelial cell [ 35 , 36 ]. ET-1 levels decrease in IDH prone patients and increase in patients who have hypertension during hemodialysis, implying its importance in regulating hemodynamic stability [ 4 ]. Consistently, we did not found a significant increase of ET-1 levels during hemodialysis in these hypotension-prone patients during the observation period, suggesting a lack of adequate vasoconstrictive response.

Similarly, we found that KRG treatment led to more activation of PRA and AngII during hemodialysis, indicating a gradually restoration of neurohormonal and cardiovascular responses to acute plasma volume change.

Although NT concentrations is an indirect measurement of NO and can be removed by dialysis [ 4 ], we observed a significant decrease in the posthemodialysis NT levels after KRG treatment group A. Previous studies have shown that hypotension-prone patients have higher baseline AngII levels compared to hypotension resistant dialysis patients [ 37 ].

This indicates that renin-angiotensin-aldosterone system may be abnormally activated in patients with recurrent IDH but still incapable to have adequate cardiovascular capacitance to the dialytic ultrafiltration. Elevation of AngII may lead to endothelial dysfunction and increase the risk of adverse cardiovascular events [ 38 ]. Despite the promising results obtained in this trial, several limitations should be acknowledged. First, the study had a relative small sample size, and further studies are needed to confirm the results.

Second, the study is a phase I pilot study, and we could only observe the differences within the same patient although this also help to eliminate the variation of blood pressure changes among different patients. Third, the long-term effects of KRG in hemodialysis patients were not studied, and further investigations are warranted.

KRG treatment improves the compensatory response to acute volume change during hemodialysis via activation of vasoconstrictors ET-1 and AngII. This is an open access article distributed under the Creative Commons Attribution License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Article of the Year Award: Outstanding research contributions of , as selected by our Chief Editors.

Read the winning articles. Journal overview. Special Issues. Academic Editor: Myeong Soo Lee. Received 05 Nov Revised 21 Jan Accepted 21 Jan Published 08 May Abstract Introduction. Material and Methods 2. Figure 1. Flow chart of patient recruitment.

Patients aged from 20 to 80 year old on thrice-weekly hemodialysis, with a treatment time of at least minutes and had at least three symptomatic episodes of intradialytic hypotension IDH in the 30 days preceding enrollment, were enrolled in the study.

Table 1. Table 2. Comparison of body weights and ultrafiltration rates with and without Korean red ginseng treatment. Figure 2. Phase I is the control phase grey boxes. The number of sessions disturbed by symptomatic IDH reduced significantly after KRG treatment in both group A hypertensive at baseline, , and group B normotensive or hypotensive at baseline, ,.

Data are shown as box and whisker plots. Horizontal lines represent median values. The boxes encompass the first and 3rd quartile of the included data. Table 3. Comparison of blood pressure measurements during hemodialysis with and without Korean red ginseng treatment.

Table 4. Changes of blood pressure during hemodialysis with and without Korean red ginseng treatment. Figure 3. The ET-1 levels increased significantly after hemodialysis in phase II in both group A hypertensive at baseline, , and group B normotensive or hypotensive at baseline, ,. The levels of NT decreased significantly after dialysis in all groups in both phases.

Hct: hematocrit; Hb: hemoglobin; Ca: calcium; P: phosphate; K: potassium. Table 5. This should be addressed considering the potential overlap between the prevalence of ginseng use and hypertension. We undertook a single centre, randomized, controlled, double-blinded, crossover trial to determine the effect of North American ginseng NAG on hour BP and renal function.

This was followed by an 8-week washout, and a subsequent week period in which the opposite treatment was consumed. At run-in, and at weeks 0 and 12 of each treatment period, participants were fitted with an ambulatory BP monitor to assess hour BP and serum cystatin C was measured. Talk with your doctor and family members or friends about deciding to join a study.

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Hide glossary Glossary Study record managers: refer to the Data Element Definitions if submitting registration or results information. Search for terms. Save this study. Warning You have reached the maximum number of saved studies The Effect of North American Ginseng on Blood Pressure in Individuals With Hypertension The safety and scientific validity of this study is the responsibility of the study sponsor and investigators.

Search for terms. Save this study. Warning You have reached the maximum number of saved studies Listing a study does not mean it has been evaluated by the U. Federal Government. Read our disclaimer for details. Last Update Posted : August 7, Study Description. The purpose of this study is to determine Korean red ginseng KRG treatment could decrease central blood pressure in subjects with hypertension. Detailed Description:.