Effects of Quercetin Treatment on Vascular Function in Deoxycorticosterone Acetate-Salt Hypertensive Rats. Comparative Study with Verapamil

Galisteo, Milagros; García-Saura, María Francisca; Jiménez, Rosario; Villar, Inmaculada Concepción; Wangensteen, Rosemary; Zarzuelo, Antonio; Vargas, Félix; Duarte, Juan

doi:10.1055/s-2004-818945

Cited by 51 publications

(13 citation statements)

References 18 publications

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“…Quercetin, the most important dietary flavonol, present in multiple fruits and vegetables, reduces blood pressure in hypertensive animals and human after chronic consumption [9], [13], [31]–[37]. Herein, we show for the first time that the conjugated derivatives Q3GA and I3GA can exert antihypertensive effects when administered intravenously.…”

Section: Discussionmentioning

confidence: 76%

Glucuronidated Quercetin Lowers Blood Pressure in Spontaneously Hypertensive Rats via Deconjugation

et al. 2012

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BackgroundChronic oral quercetin reduces blood pressure and restores endothelial dysfunction in hypertensive animals. However, quercetin (aglycone) is usually not present in plasma, because it is rapidly metabolized into conjugated, mostly inactive, metabolites. The aim of the study is to analyze whether deconjugation of these metabolites is involved in the blood pressure lowering effect of quercetin.Methodology/Principal FindingsWe have analyzed the effects on blood pressure and vascular function in vitro of the conjugated metabolites of quercetin (quercetin-3-glucuronide, Q3GA; isorhamnetin-3-glucuronide, I3GA; and quercetin-3′-sulfate, Q3'S) in spontaneously hypertensive rats (SHR). Q3GA and I3GA (1 mg/kg i.v.), but not Q3'S, progressively reduced mean blood pressure (MBP), measured in conscious SHR. The hypotensive effect of Q3GA was abolished in SHR treated with the specific inhibitor of β-glucuronidase, saccharic acid 1,4-lactone (SAL, 10 mg/ml). In mesenteric arteries, unlike quercetin, Q3GA had no inhibitory effect in the contractile response to phenylephrine after 30 min of incubation. However, after 1 hour of incubation Q3GA strongly reduced this contractile response and this effect was prevented by SAL. Oral administration of quercetin (10 mg/Kg) induced a progressive decrease in MBP, which was also suppressed by SAL.ConclusionsConjugated metabolites are involved in the in vivo antihypertensive effect of quercetin, acting as molecules for the plasmatic transport of quercetin to the target tissues. Quercetin released from its glucuronidated metabolites could be responsible for its vasorelaxant and hypotensive effect.

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Section: Discussionmentioning

confidence: 76%

Glucuronidated Quercetin Lowers Blood Pressure in Spontaneously Hypertensive Rats via Deconjugation

et al. 2012

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“…In this ex vivo study [ 39 ], they have demonstrated that quercetin (10 −5 M) acutely potentiates vascular relaxation induced by acetylcholine in 2K1C hypertensive rats, suggesting that quercetin shows its anti-hypertensive action by diminishing elastance of blood vessels. Galisteo et al [ 40 ] have reported the action of chronic oral intake of quercetin on systolic blood pressure and vascular function in deoxycorticosterone acetate (DOCA)-salt hypertensive rats. Quercetin enhances endothelial-dependent aortic dilatations in rats developed with DOCA-salt-induced hypertension in a similar manner to verapamil, a Ca 2+ channel blocker, which reduces blood pressure [ 40 ].…”

Section: Actions Of Quercetin On Blood Pressure In Human and Modelmentioning

confidence: 99%

Actions of Quercetin, a Polyphenol, on Blood Pressure

et al. 2017

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Disorder of blood pressure control causes serious diseases in the cardiovascular system. This review focuses on the anti-hypertensive action of quercetin, a flavonoid, which is one of the polyphenols characterized as the compounds containing large multiples of phenol structural units, by varying the values of various blood pressure regulatory factors, such as vascular compliance, peripheral vascular resistance, and total blood volume via anti-inflammatory and anti-oxidant actions. In addition to the anti-inflammatory and anti-oxidant actions of quercetin, we especially describe a novel mechanism of quercetin’s action on the cytosolic Cl− concentration ([Cl−]c) and novel roles of the cytosolic Cl− i.e., (1) quercetin elevates [Cl−]c by activating Na+-K+-2Cl− cotransporter 1 (NKCC1) in renal epithelial cells contributing to Na+ reabsorption via the epithelial Na+ channel (ENaC); (2) the quercetin-induced elevation of [Cl−]c in renal epithelial cells diminishes expression of ENaC leading to a decrease in renal Na+ reabsorption; and (3) this reduction of ENaC-mediated Na+ reabsorption in renal epithelial cells drops volume-dependent elevated blood pressure. In this review, we introduce novel, unique mechanisms of quercetin’s anti-hypertensive action via activation of NKCC1 in detail.

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“…Indeed, the effects of quercitin have been extensively investigated in animal models of CVDs, especially with regard to its antihypertensive effects. For example, a reduction of blood pressure after administration of quercitin in spontaneously hypertensive rats has been showed [ 188 ], as well as in salt-hypertensive [ 189 , 190 ] and NO deficient rats [ 191 ]. Recently, it has been reported that quercitin is able to ameliorate arterial erectile dysfunctions in rats via NOS regulation restoring, almost in part, the function of NO-cGMP pathway in the process of penis erection [ 192 ].…”

Section: Polyphenols and The No Signalingmentioning

confidence: 99%

Targeting Nitric Oxide with Natural Derived Compounds as a Therapeutic Strategy in Vascular Diseases

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Damato

et al. 2016

Oxidative Medicine and Cellular Longevity

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Within the family of endogenous gasotransmitters, nitric oxide (NO) is the smallest gaseous intercellular messenger involved in the modulation of several processes, such as blood flow and platelet aggregation control, essential to maintain vascular homeostasis. NO is produced by nitric oxide synthases (NOS) and its effects are mediated by cGMP-dependent or cGMP-independent mechanisms. Growing evidence suggests a crosstalk between the NO signaling and the occurrence of oxidative stress in the onset and progression of vascular diseases, such as hypertension, heart failure, ischemia, and stroke. For these reasons, NO is considered as an emerging molecular target for developing therapeutic strategies for cardio- and cerebrovascular pathologies. Several natural derived compounds, such as polyphenols, are now proposed as modulators of NO-mediated pathways. The aim of this review is to highlight the experimental evidence on the involvement of nitric oxide in vascular homeostasis focusing on the therapeutic potential of targeting NO with some natural compounds in patients with vascular diseases.

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Effects of Quercetin Treatment on Vascular Function in Deoxycorticosterone Acetate-Salt Hypertensive Rats. Comparative Study with Verapamil

Cited by 51 publications

References 18 publications

Glucuronidated Quercetin Lowers Blood Pressure in Spontaneously Hypertensive Rats via Deconjugation

Glucuronidated Quercetin Lowers Blood Pressure in Spontaneously Hypertensive Rats via Deconjugation

Actions of Quercetin, a Polyphenol, on Blood Pressure

Targeting Nitric Oxide with Natural Derived Compounds as a Therapeutic Strategy in Vascular Diseases

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