Mechanisms involved in UTP-induced contraction in isolated rat aorta

López, Covadonga; Sánchez, Manuel; Hidalgo, Agustı́n; Boto, María José García de

doi:10.1016/s0014-2999(00)00097-2

Cited by 4 publications

(5 citation statements)

References 10 publications

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“…It has been reported that external Ca 2ϩ (16,18,29) and intracellular Ca 2ϩ stores can contribute to the increase in [Ca 2ϩ ] i in response to UTP (9,18,20,30). In the present study, Up 4 A-induced vasoconstriction was inhibited by sequestration of extracellular Ca 2ϩ with EGTA (Fig.…”

Section: Discussionsupporting

confidence: 59%

“…9,20,28). The increase in [Ca 2ϩ ] i in response to UTP can result from Ca 2ϩ entry from the extracellular space (28) and release from intracellular stores (16,20,30).…”

mentioning

confidence: 99%

“…9,20,28). The increase in [Ca 2ϩ ] i in response to UTP can result from Ca 2ϩ entry from the extracellular space (28) and release from intracellular stores (16,20,30). In addition, it has been reported that P2Y receptormediated aortic contraction involves the RhoA/Rho kinase pathway (13,32).…”

mentioning

confidence: 99%

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Up₄A stimulates endothelium-independent contraction of isolated rat pulmonary artery

Gui¹,

Walsh²,

Jankowski³

et al. 2008

American Journal of Physiology-Lung Cellular and Molecular Phys

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Extracellular nucleotides, such as ATP, UDP, and UTP, regulate pulmonary vascular tone through P2X and P2Y receptors. Recently, uridine adenosine tetraphosphate (Up(4)A) was reported as a novel endothelium-derived vasoconstrictive factor. Up(4)A contains both purine and pyrimidine moieties, which potentially activate P2X and P2Y receptors. The present study examined the effect of Up(4)A on contractility of isolated rat pulmonary artery. Up(4)A at 1-100 microM stimulated contraction in a concentration-dependent manner. Up(4)A was equipotent as UTP and UDP in the endothelium-denuded artery while much more effective than UTP and UDP in endothelium-intact preparations. The vasoconstrictor effect of Up(4)A was inhibited by suramin but not IP(5)I or desensitization of P2X receptors with alpha,beta-methylene-ATP (alpha,beta-Me-ATP). Up(4)A-induced contraction was also inhibited by pretreatment with thapsigargin, nitrendipine, or EGTA but unaffected by H1152. Furthermore, unlike ATP and UTP, Up(4)A did not induce relaxation of endothelium-intact preparations precontracted with phenylephrine. These results suggest that Up(4)A is a potent vasoconstrictor, but not a vasodilator, of the rat pulmonary artery. Up(4)A likely acts through a suramin-sensitive P2Y receptor. The contractile effect of Up(4)A involves the entry of extracellular Ca(2+) and release of Ca(2+) from intracellular stores but not Ca(2+) sensitization via the RhoA/Rho kinase pathway. Up(4)A, therefore, potentially plays an important role in the regulation of pulmonary vascular tone.

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Section: Discussionsupporting

confidence: 59%

“…9,20,28). The increase in [Ca 2ϩ ] i in response to UTP can result from Ca 2ϩ entry from the extracellular space (28) and release from intracellular stores (16,20,30).…”

mentioning

confidence: 99%

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Up₄A stimulates endothelium-independent contraction of isolated rat pulmonary artery

Gui¹,

Walsh²,

Jankowski³

et al. 2008

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…It was reported that UTP-induced contraction involves the activation of PKC in rat aorta (Lopez et al, 2000). We hypothesized that PKC activation is involved in this contractile potentiation by nicotine, and PKC activities in the artery were actually measured.…”

Section: Discussionmentioning

confidence: 99%

“…We have previously shown that PKC plays a pivotal role in the regulation of cerebral arterial tone (Nishizawa et al, 1992a(Nishizawa et al, , b, 1996 in the canine basilar artery. It was reported that UTP-induced contraction involves the activation of PKC in rat aorta (Lopez et al, 2000). We hypothesized that PKC activation is involved in this contractile potentiation by nicotine, and PKC activities in the artery were actually measured.…”

Section: Discussionmentioning

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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Mesaconitine-induced relaxation in rat aorta: involvement of Ca2+ influx and nitric-oxide synthase in the endothelium

Mitamura

Horie

Sakaguchi

et al. 2002

European Journal of Pharmacology

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Mechanisms involved in UTP-induced contraction in isolated rat aorta

Cited by 4 publications

References 10 publications

Up₄A stimulates endothelium-independent contraction of isolated rat pulmonary artery

Up₄A stimulates endothelium-independent contraction of isolated rat pulmonary artery

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

Mesaconitine-induced relaxation in rat aorta: involvement of Ca2+ influx and nitric-oxide synthase in the endothelium

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Mechanisms involved in UTP-induced contraction in isolated rat aorta

Cited by 4 publications

References 10 publications

Up4A stimulates endothelium-independent contraction of isolated rat pulmonary artery

Up4A stimulates endothelium-independent contraction of isolated rat pulmonary artery

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

Mesaconitine-induced relaxation in rat aorta: involvement of Ca2+ influx and nitric-oxide synthase in the endothelium

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Up₄A stimulates endothelium-independent contraction of isolated rat pulmonary artery

Up₄A stimulates endothelium-independent contraction of isolated rat pulmonary artery