Chronic ethanol consumption enhances inducible endothelium-dependent hyperpolarizing factor-mediated relaxation in the rat artery

Yuui, Katsuya; Kudo, Risa; Kasuda, Shogo; Hatake, Kiyohiko

doi:10.1016/j.ejphar.2019.172759

Cited by 4 publications

(5 citation statements)

References 26 publications

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“…For instance, it is known that the inducible endothelium-dependent hyperpolarizing factor (iEDHF) pathway is activated as a compensatory response to ethanol-induced hypercontractility. In rats chronically treated with ethanol, acetylcholine-induced relaxation of mesenteric arteries was significantly greater compared to control arteries and inhibitors of EDHF reversed this response [65].…”

Section: The Myogenic Theorymentioning

confidence: 86%

Reactive Oxygen Species Are Central Mediators of Vascular Dysfunction and Hypertension Induced by Ethanol Consumption

Padovan,

Dourado,

Pimenta

et al. 2023

Antioxidants

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Consumption of high amounts of ethanol is a risk factor for development of cardiovascular diseases such as arterial hypertension. The hypertensive state induced by ethanol is a complex multi-factorial event, and oxidative stress is a pathophysiological hallmark of vascular dysfunction associated with ethanol consumption. Increasing levels of reactive oxygen species (ROS) in the vasculature trigger important processes underlying vascular injury, including accumulation of intracellular Ca2+ ions, reduced bioavailability of nitric oxide (NO), activation of mitogen-activated protein kinases (MAPKs), endothelial dysfunction, and loss of the anticontractile effect of perivascular adipose tissue (PVAT). The enzyme nicotinamide adenine dinucleotide phosphate (NADPH) oxidase plays a central role in vascular ROS generation in response to ethanol. Activation of the renin–angiotensin–aldosterone system (RAAS) is an upstream mechanism which contributes to NADPH oxidase stimulation, overproduction of ROS, and vascular dysfunction. This review discusses the mechanisms of vascular dysfunction induced by ethanol, detailing the contribution of ROS to these processes. Data examining the association between neuroendocrine changes and vascular oxidative stress induced by ethanol are also reviewed and discussed. These issues are of paramount interest to public health as ethanol contributes to blood pressure elevation in the general population, and it is linked to cardiovascular conditions and diseases.

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Section: The Myogenic Theorymentioning

confidence: 86%

Reactive Oxygen Species Are Central Mediators of Vascular Dysfunction and Hypertension Induced by Ethanol Consumption

Padovan,

Dourado,

Pimenta

et al. 2023

Antioxidants

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“…Subsequently, the vascular function was assessed by measuring the vascular isometric force, as reported previously. 14,15 SMA was sectioned into rings 1–1.5 mm long. The rings were horizontally mounted on 50-μm-diameter tension hooks in 4-mL organ baths containing Krebs–Ringer solution (118 mM NaCl, 4.7 mM KCl, 1.2 mM MgSO 4 , 1.2 mM KH 2 PO 4 , 25 mM NaHCO 3 , 2.5 mM CaCl 2 , and 10 mM D -glucose; pH 7.4).…”

Section: Methodsmentioning

confidence: 99%

“…The resting tension was maintained at 0.2 g throughout the experiment. 15 To examine the role of the endothelium in IL-1β–induced contraction and relaxation, it was denuded by gently rubbing the intimal surface with a stainless-steel wire. Removal of the endothelium was confirmed by the loss of relaxation in response to 10–6 M acetylcholine.…”

Section: Methodsmentioning

confidence: 99%

Arterial thromboxane A2-induced transient contraction after IL-1β exposure

2022

Self Cite

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The involvement of thromboxane A2 (TXA2) in systemic inflammation and infection is well recognized. However, there are few reports on the involvement of prostanoids in warm shock (the initial pathology of sepsis). Previous studies showed that interleukin (IL)-1β causes a rapid inducible nitric oxide synthase/nitric oxide (iNOS/NO)-mediated relaxation in peripheral blood vessels during warm shock. Furthermore, a transient contraction was seen before this relaxation occurred. The present study aimed to elucidate the mechanism of this transient contraction. We measured isometric tension changes in the superior mesenteric arteries from normal male Wistar rats by adding IL-1β at the point of maximum contraction by phenylephrine (Ph). The same study was performed for each vessel pretreated with various inhibitors, including SQ29548, a TXA2 receptor antagonist, 30 min before Ph contraction. In addition, the concentration of thromboxane B2 (TXB2) in SMA was measured by probe electrospray ionization. Treatment of endothelial vessels with cyclooxygenase 1 (COX1)/2 inhibitors SC560/NS398 and TXA2 receptor antagonist SQ29548 suppressed IL-1β–induced transient contractions. This transient contraction reaction was derived from TXA2. Additionally, gene expression of COX2/TXA2 synthetase and the concentration of TXB2 were significantly increased in IL-1β-exposed vessels. It was demonstrated for the first time in inflamed blood vessels that endothelial cell-derived COX2/TXA2 is induced before iNOS and causes transient contractions. TXA2 may be considered an early sign of warm shock or as a biological defense mechanism in the early stages of septic shock.

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“…Both ethanol and acetaldehyde have been shown to evoke dilation of intact superior mesenteric arteries (SMA) ( 28 , 134 , 138 ). Acetaldehyde-mediated vasodilation, however, was more potent than that of ethanol ( 28 ).…”

Section: Muscle Types and Their Mechanisms For Contractionmentioning

confidence: 99%

“…Acetaldehyde-mediated vasodilation, however, was more potent than that of ethanol ( 28 ). A central role for the endothelium in ethanol-induced dilation of mesenteric arteries is underscored by data from Yuui et al (2019) ( 138 ) who showed that chronic administration of moderate levels of ethanol to rats enhanced the activity of an endothelium-dependent hyperpolarizing factor (EDHF) pathway, thereby promoting vascular relaxation. In addition, Jin et al (2019) ( 28 ) showed that ethanol dilation of intact SMA may be mediated through the activity of NO • and guanylyl cyclase, the latter being a main target of EDHF.…”

Section: Muscle Types and Their Mechanisms For Contractionmentioning

confidence: 99%

Alcohol Use Disorders and Their Harmful Effects on the Contractility of Skeletal, Cardiac and Smooth Muscles

Alleyne¹,

Dopico²

2021

Adv. Drug Alcohol Res.

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Alcohol misuse has deleterious effects on personal health, family, societal units, and global economies. Moreover, alcohol misuse usually leads to several diseases and conditions, including alcoholism, which is a chronic condition and a form of addiction. Alcohol misuse, whether as acute intoxication or alcoholism, adversely affects skeletal, cardiac and/or smooth muscle contraction. Ethanol (ethyl alcohol) is the main effector of alcohol-induced dysregulation of muscle contractility, regardless of alcoholic beverage type or the ethanol metabolite (with acetaldehyde being a notable exception). Ethanol, however, is a simple and “promiscuous” ligand that affects many targets to mediate a single biological effect. In this review, we firstly summarize the processes of excitation-contraction coupling and calcium homeostasis which are critical for the regulation of contractility in all muscle types. Secondly, we present the effects of acute and chronic alcohol exposure on the contractility of skeletal, cardiac, and vascular/ nonvascular smooth muscles. Distinctions are made between in vivo and in vitro experiments, intoxicating vs. sub-intoxicating ethanol levels, and human subjects vs. animal models. The differential effects of alcohol on biological sexes are also examined. Lastly, we show that alcohol-mediated disruption of muscle contractility, involves a wide variety of molecular players, including contractile proteins, their regulatory factors, membrane ion channels and pumps, and several signaling molecules. Clear identification of these molecular players constitutes a first step for a rationale design of pharmacotherapeutics to prevent, ameliorate and/or reverse the negative effects of alcohol on muscle contractility.

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Chronic ethanol consumption enhances inducible endothelium-dependent hyperpolarizing factor-mediated relaxation in the rat artery

Cited by 4 publications

References 26 publications

Reactive Oxygen Species Are Central Mediators of Vascular Dysfunction and Hypertension Induced by Ethanol Consumption

Reactive Oxygen Species Are Central Mediators of Vascular Dysfunction and Hypertension Induced by Ethanol Consumption

Arterial thromboxane A2-induced transient contraction after IL-1β exposure

Alcohol Use Disorders and Their Harmful Effects on the Contractility of Skeletal, Cardiac and Smooth Muscles

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