Nicotine-Induced Contraction in the Rat Coronary Artery: Possible Involvement of the Endothelium, Reactive Oxygen Species and COX-1 Metabolites

Kurahashi, Kazuyoshi; Shirahase, Hiroaki; Nakamura, Shohei; Tarumi, Tadaaki; Koshino, Yasuaki; Ai-min, Wang; Nishihashi, Tsuyoshi; Shimizu, Yuma

doi:10.1097/00005344-200110001-00006

Cited by 7 publications

(5 citation statements)

References 18 publications

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“…The involvement of 5‐LOX metabolites in the EDC was ruled out because the selective 5‐LOX inhibitor ZM‐230487 did not affect EDC 20 . Along with the results of the present study, we have reported recently that, in the rat coronary artery, the nicotine‐induced EDC is mediated by the COX metabolites of arachidonic acid in the presence of l ‐NAME and arachidonic acid 8 …”

Section: Discussionsupporting

confidence: 77%

“…This augmentation may be due to loss of EDR and domination of direct stimulation of α‐adrenoceptors on the arterial smooth muscle. In contrast, such treatment attenuates nicotine‐induced contraction in the rat coronary artery in the presence of l ‐NAME and arachidonic acid 8 . The attenuation may be due to the simultaneous inhibition of EDR and EDC.…”

Section: Discussionmentioning

confidence: 92%

“…1a). Arachidonic acid metabolites, including TXA 2 , in the canine basilar artery, leukotrienes in the rabbit coronary artery and cyclo‐oxygenase (COX)‐1 metabolites in the rat coronary artery are considered to be possible derived EDCF 5,7,8 . The presence of arachidonic acid (1 µmol/L) slightly, albeit not significantly, augmented the contractions to 0.003–1 µmol/L NA (Fig.…”

Section: Resultsmentioning

confidence: 98%

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Involvement of Endothelial Cyclo‐oxygenase Metabolites in Noradrenaline‐induced Contraction of Rat Coronary Artery

Wang¹,

Nishihashi²,

Trandafir³

et al. 2005

Clin Exp Pharma Physio

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1. Noradrenaline (NA; 0.3 micromol/L) caused a contraction of the rat coronary artery that markedly increased in the presence of the nitric oxide synthase (NOS) inhibitor N(G)-nitro-l-arginine methyl ester (L-NAME; 100 micromol/L) and arachidonic acid (1 micromol/L; P < 0.05). 2. The present experiments attempted to elucidate the endothelium dependency of the contraction and to pharmacologically characterize the factors involved in the contraction induced by NA (0.3 micromol/L) in the presence of L-NAME and arachidonic acid in ring preparations of the rat coronary artery. 3. The NA (0.3 micromol/L)-induced contraction was attenuated by a chemical remover of the endothelium (saponin at concentrations of 0.1 and 0.4 mg/mL) in a concentration-dependent manner (P < 0.05). 4. The cyclo-oxygenase (COX)-1 inhibitor flurbiprofen (0.01-1 micromol/L) and the COX-2 inhibitor nimesulide (0.01-1 micromol/L) attenuated the NA-induced contraction in a concentration-dependent manner and the inhibitory effect of flurbiprofen was significantly more potent than that of nimesulide (P < 0.05). The 5-lipoxigenase inhibitor ZM-230487 (1 micromol/L) did not affect the NA-induced contraction. 5. The thromboxane A2 (TXA2) synthetase inhibitor OKY-046 (30 micromol/L) and the TXA2 antagonist S-1452 (0.1-10 micromol/L) did not attenuate the NA-induced contraction. 6. These results indicate that the contraction induced by NA in the rat coronary artery in the presence of L-NAME and arachidonic acid is endothelium dependent and is due to endothelial COX metabolites of arachidonic acid.

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Section: Discussionsupporting

confidence: 77%

Section: Discussionmentioning

confidence: 92%

Section: Resultsmentioning

confidence: 98%

See 1 more Smart Citation

Involvement of Endothelial Cyclo‐oxygenase Metabolites in Noradrenaline‐induced Contraction of Rat Coronary Artery

Wang¹,

Nishihashi²,

Trandafir³

et al. 2005

Clin Exp Pharma Physio

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“…Indeed, Na ϩ entry can activate or contribute to the production of oxygen-derived free radicals (12), which may mediate the damage of endothelial-dependent vasoreactivity induced by nicotine (16,17). Furthermore, nicotine-induced contraction of the rat coronary artery in the presence of N-nitro-L-arginine methyl ester has been shown to be endothelium dependent and involve reactive oxygen species and cyclooxygenase 1 metabolites of arachidonic acid (13). The mitogenic effect of nicotine could also be stimulated by the Na ϩ flux mediated by nAChRs, as Na ϩ entry has been suggested to be a necessary event to elicit DNA synthesis in several cell types (11,25).…”

Section: Discussionmentioning

confidence: 99%

Expression and function of neuronal nicotinic ACh receptors in rat microvascular endothelial cells

Moccia¹,

Frost²,

Berra‐Romani³

et al. 2004

American Journal of Physiology-Heart and Circulatory Physiology

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The expression and function of nicotinic ACh receptors (nAChRs) in rat coronary microvascular endothelial cells (CMECs) were examined using RT-PCR and whole cell patch-clamp recording methods. RT-PCR revealed expression of mRNA encoding for the subunits alpha(2), alpha(3), alpha(4), alpha(5), alpha(7), beta(2), and beta(4) but not beta(3). Focal application of ACh evoked an inward current in isolated CMECs voltage clamped at negative membrane potentials. The current-voltage relationship of the ACh-induced current exhibited marked inward rectification and a reversal potential (E(rev)) close to 0 mV. The cholinergic agonists nicotine, epibatidine, and cytisine activated membrane currents similar to those evoked by ACh. The nicotine-induced current was abolished by the neuronal nAChR antagonist mecamylamine. The direction and magnitude of the shift in E(rev) of nicotine-induced current as a function of extracellular Na(+) concentration indicate that the nAChR channel is cation selective and follows that predicted by the Goldman-Hodgkin-Katz equation assuming K(+)/Na(+) permeability ratio of 1.11. In fura-2-loaded CMECs, application of ACh, but not of nicotine, elicited a transient increase in intracellular free Ca(2+) concentration. Taken together, these results demonstrate that neuronal nAChR activation by cholinergic agonists evokes an inward current in CMECs carried primarily by Na(+), which may contribute to the plasma nicotine-induced changes in microvascular permeability and reactivity induced by elevations in plasma nicotine.

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“…A high concentration of nicotine causes dosedependent constriction in some arteries (Kurahashi et al, 2001;Shirahase et al, 1988). However, a high concentration of nicotine also induces transitory vasodilatation in precontracted arteries via the perivascular nitroxidergic nerve (Toda, 1975).…”

Section: Introductionmentioning

confidence: 99%

Nicotine Exposure, Mimicked Smoking, Directly and Indirectly Enhanced Protein Kinase C Activity in Isolated Canine Basilar Artery, Resulting in Enhancement of Arterial Contraction

Koide

Nishizawa

Yamamoto

et al. 2005

J Cereb Blood Flow Metab

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Cigarette smoking is a significant risk factor in the incidence of cerebrovascular disorders. Among the many compounds in cigarette smoke, nicotine is considered to most significantly affect cerebral arterial tone. The purpose of this study is to investigate precise pharmacological effects of nicotine on the regulation of cerebral arterial tone. To mimic smoking, a low concentration of nicotine (10 À6 mol/L), which is equivalent to the serum level of habitual smokers, was treated for 1 hour in an isometric tension study and for 24 hours in a study using cultured vascular endothelial cells (VECs). Using the canine basilar artery, the effect of nicotine on uridine 5 0 -triphosphate (UTP)-induced vasoconstriction was examined in the isometric tension study. Protein kinase C (PKC) activity in the canine basilar artery was measured by enzyme immunoassay. Endothelial function was assessed by endothelium-dependent vasodilatation and endogenous nitric oxide (NO) synthesis in VECs using a fluorescent indicator, diaminofluorescein-FM diacetate (DAF-FM/DA). Nicotine significantly enhanced UTP-induced contraction and PKC activity in the artery, and attenuated endotheliumdependent vasodilatation and NO synthesis in VECs. Because PKC activity was increased by deendothelialization itself, endothelial dysfunction by nicotine enhances PKC activity. Because PKC was further activated by nicotine even in the de-endothelialized artery, nicotine directly affects PKC activities in smooth muscle. These results indicate that nicotine potentiates contractile response through direct and indirect PKC activation in the canine basilar artery.

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Nicotine-Induced Contraction in the Rat Coronary Artery: Possible Involvement of the Endothelium, Reactive Oxygen Species and COX-1 Metabolites

Cited by 7 publications

References 18 publications

Involvement of Endothelial Cyclo‐oxygenase Metabolites in Noradrenaline‐induced Contraction of Rat Coronary Artery

Involvement of Endothelial Cyclo‐oxygenase Metabolites in Noradrenaline‐induced Contraction of Rat Coronary Artery

Expression and function of neuronal nicotinic ACh receptors in rat microvascular endothelial cells

Nicotine Exposure, Mimicked Smoking, Directly and Indirectly Enhanced Protein Kinase C Activity in Isolated Canine Basilar Artery, Resulting in Enhancement of Arterial Contraction

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