Angiotensin II type 1 (AT1)-receptor blocker prevents impairment of endothelium-dependent cerebral vasodilation by acute cigarette smoking in rats

Iida, Hiroki; Iida, Mami; Takenaka, Motoyasu; Fujiwara, Hisayoshi; Dohi, Shuji

doi:10.1016/j.lfs.2005.07.004

Cited by 18 publications

(11 citation statements)

References 44 publications

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“…In the present study, on rats in vivo: (a) acute singlecigarette smoking caused an impairment of endotheliumdependent vasodilation in cerebral vessels, as in our previous study [7,8], and (b) pretreatment with cilostazol, but not with aspirin, prevented this effect. To judge from these data, although each of these drugs can be used for antiplatelet therapy, they differ greatly in their ability to protect cerebral endothelial function against the effects of cigarette smoking.…”

Section: Discussionsupporting

confidence: 76%

“…Oxidative stress is believed to play a critical role in the development of the smoking-induced impairment of endothelium-dependent vasodilation [7,8]. Cilostazol reportedly increases the basal production of NO from endothelial cells [20], leading to a restoration of NO bioavailability.…”

Section: Discussionmentioning

confidence: 99%

“…In this study, cigarette smoking was performed by the rat inhaling 60 puffs per min of mainstream cigarette smoke for 1 min (1 mg-nicotine cigarette; Marlboro, Philip Morris) [7,8,18]. Each animal inspired the mainstream smoke through its tracheal cannula (by way of the ventilator).…”

Section: Experimental Protocolsmentioning

confidence: 99%

“…Several studies have shown that smoking or tobacco products can produce functional alterations in the endothelium, leading to impaired endothelium-dependent dilation in peripheral or cerebral vessels [4][5][6]. We previously reported that an angiotensin II (Ang II) type 1 (AT1)-receptor blocker (valsartan), a Rho-kinase inhibitor (fasudil), or an NADPH oxidase inhibitor (apocynin) could prevent this impairment [7,8]. Thus, oxidative stress may make a major contribution to the endothelial dysfunction in cerebral vessels that is induced by acute smoking.…”

Section: Introductionmentioning

confidence: 99%

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Comparative effects of cilostazol and aspirin on the impairment of endothelium-dependent cerebral vasodilation caused by acute cigarette smoking in rats

Iida

Takenaka

et al. 2009

J Thromb Thrombolysis

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We previously reported that acute cigarette smoking can cause a dysfunction of endothelium-dependent vasodilation in cerebral vessels, and that a reduction of oxidative stress by agents such as valsartan, fasudil, or apocynin prevented this impairment. Here, our aim was to investigate the comparative effects of two antiplatelet drugs used for stroke-prevention [a phosphodiesterase-3 inhibitor (cilostazol) and a cyclooxygenase inhibitor (aspirin)] on smoking-induced endothelial dysfunction in cerebral arterioles. In Sprague-Dawley rats, we used a closed cranial window preparation to measure the changes in pial vessel diameters induced by topical application of acetylcholine (ACh) following intraperitoneal injection of 0.5% carboxymethyl cellulose sodium salt (CMC; vehicle control for the antiplatelet drugs). After 1-min smoking (1 mg-nicotine cigarette), the arteriolar responses to ACh were reexamined. Finally, after intraperitoneal cilostazol or aspirin (each in 0.5% CMC) pretreatment, we reexamined the vasodilator responses to topical ACh (before and after cigarette smoking). Under control conditions, cerebral arterioles were dose-relatedly dilated by topical ACh (10(-6) and 10(-5 )M). One hour after 1-min smoking, 10(-5 )M ACh (a) constricted cerebral pial arterioles in the control group and in the aspirin-pretreatment group (responses not significantly different from each other), but (b) dilated cerebral pial arteries in the cilostazol pretreatment groups (responses significantly different from those obtained without cilostazol pretreatment). Thus, cilostazol (but not aspirin) may prevent the smoking-induced impairment of endothelium-dependent vasodilation in cerebral pial arterioles.

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Section: Discussionsupporting

confidence: 76%

Section: Discussionmentioning

confidence: 99%

Section: Experimental Protocolsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Comparative effects of cilostazol and aspirin on the impairment of endothelium-dependent cerebral vasodilation caused by acute cigarette smoking in rats

Iida

Takenaka

et al. 2009

J Thromb Thrombolysis

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“…In addition to hypertension, ANG II and activation of AT 1 receptors contribute to vascular disease under conditions without coexisting hypertension, including aging (199), diabetes (11,270), atherosclerosis (59, 227), and in response to cigarette smoking (129). Increases in superoxide as well as impairment Fig.…”

Section: Pleiotropic Effects Of Angiotensin IImentioning

confidence: 99%

Protecting against vascular disease in brain

Faraci

2011

American Journal of Physiology-Heart and Circulatory Physiology

164

238

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Endothelial cells exert an enormous influence on blood vessels throughout the circulation, but their impact is particularly pronounced in the brain. New concepts have emerged recently regarding the role of this cell type and mechanisms that contribute to endothelial dysfunction and vascular disease. Activation of the renin-angiotensin system plays a prominent role in producing these abnormalities. Both oxidative stress and local inflammation are key mechanisms that underlie vascular disease of diverse etiology. Endogenous mechanisms of vascular protection are also present, including antioxidants, anti-inflammatory molecules, and peroxisome proliferator-activated receptor-γ. Despite their clear importance, studies of mechanisms that underlie cerebrovascular disease continue to lag behind studies of vascular biology in general. Identification of endogenous molecules and pathways that protect the vasculature may result in targeted approaches to prevent or slow the progression of vascular disease that causes stroke and contributes to the vascular component of dementia and Alzheimer's disease.

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Preventive effect of varenicline on impairment of endothelial function in cerebral vessels induced by acute smoking in rats

Iida

Takenaka

et al. 2012

J Anesth

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Preoperative smoking cessation is important for recovery from surgery without complications. Available evidence suggests nicotine replacement therapy could be safe and effective in the perioperative period. On the other hand, the newly developed selective nicotinic acetylcholine (ACh) receptor partial agonist, varenicline tartrate, is also effective as an aid for smoking cessation and helps people to stop smoking. During the transitional phase between the decision to stop smoking and actual smoking cessation, patients could use varenicline before undertaking smoking cessation. We have previously reported that acute cigarette smoking can cause impairment of endothelium-dependent vasodilation in cerebral vessels; thus, the use of varenicline before surgery in a patient who is still a smoker may not be safe with regard to endothelial function. Therefore, to assess the safety of varenicline in terms of endothelial function, we evaluated its effect on the acute smoking-induced impairment of endothelium-dependent cerebral vasodilation. In anesthetized Sprague-Dawley rats, we applied ACh topically to pial vessels; then, after administering intravenous varenicline or saline injection, we reexamined the ACh-induced vasodilator response both before and after smoking. Under control conditions, cerebral pial arterioles were dose-relatedly dilated by ACh. After smoking, 10(-5) M ACh constricted the arterioles following saline pretreatment (diameter -7.6 ± 1.8 %, n = 6), but induced dilation following varenicline pretreatment (diameter +15.3 ± 3.3 %, n = 6). Thus, varenicline may prevent the smoking-induced impairment of endothelium-dependent vasodilation in cerebral pial arterioles.

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Angiotensin II type 1 (AT1)-receptor blocker prevents impairment of endothelium-dependent cerebral vasodilation by acute cigarette smoking in rats

Cited by 18 publications

References 44 publications

Comparative effects of cilostazol and aspirin on the impairment of endothelium-dependent cerebral vasodilation caused by acute cigarette smoking in rats

Comparative effects of cilostazol and aspirin on the impairment of endothelium-dependent cerebral vasodilation caused by acute cigarette smoking in rats

Protecting against vascular disease in brain

Preventive effect of varenicline on impairment of endothelial function in cerebral vessels induced by acute smoking in rats

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