Prostacyclin and thromboxane release from the vessel wall — Comparison between an incubation and a perfusion model

Brunkwall, Jan; Bergqvist, David; Stjernquist, U

doi:10.1016/0090-6980(87)90092-x

Cited by 13 publications

(2 citation statements)

References 22 publications

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“…Such discrepancies indicate that, at least in studies of vasoconstrictor mechanisms, the perfused mesenteric bed provides different results from the isolated mesenteric arteries. Moreover, Brunkwall, Bergqvist & Sternquist (1987), in rabbit vessels, and Mehta & Roberts (1983), in human umbilical veins, found no correlation in prostaglandin release between isolated and perfused vascular preparations.…”

Section: Discussionmentioning

confidence: 86%

Effects of eicosanoids and nitric oxide on the noradrenaline‐induced contractions in the rat mesenteric bed

Peredo

Adler‐Graschinsky

2000

J. Autonom. Pharmacol.

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1. The effects of the inhibition of the metabolism of arachidonic acid (AA) on the constrictor responses to noradrenaline (NA) were studied in the rat perfused mesenteric bed. The inhibitor of all the pathways of AA metabolism, 10 microM eicosatetraynoic acid (ETYA), reduced the constrictor responses to all the concentrations of NA assayed. 2. The constrictor responses to NA were also reduced by the cyclooxygenase (COX) inhibitor, indomethacin (10 microM), as well as by the lipoxygenase inhibitor, nordihidroguaiaretic acid (1 microM; NDGA), whereas they were unmodified by the cytochrome P450 monooxigenase inhibitors, clotrimazole (10 microM), metyrapone (10 microM) and proadifen (10 microM). 3. The reduction in NA contractility induced by indomethacin was reverted with a decreasing order of potency by the thromboxane A2 analogue, U-46619 > prostaglandin (PG) E2 > PGF2alpha. The exposure of the mesenteric bed to NA increased the production of PGF2alpha, whereas it did not modify the production of the remaining AA metabolites. 4. The increase in the NA-induced contractions caused by endothelium removal, as well as by the inhibition of nitric oxide synthase (NOs) with NG-nitro-L-arginine methyl ester (400 microM; L-NAME), was suppressed by indomethacin but not by NDGA. These observations suggest that the lipoxygenase-derived metabolites are formed in the endothelium, whereas the COX-derived metabolites are formed in the vascular smooth muscle. 5. The TP receptor antagonist, SQ29548, did not modify the NA-induced contractions, either in the presence or in the absence of the endothelium. 6. Contractions elicited by KCI (60-100 mM) were unmodified by the AA metabolism inhibitors, ETYA, NDGA and indomethacin. 7. In summary, these results show that metabolites of AA, through both the COX and the lipoxygenase pathways, are involved in the NA-induced contractions in the rat mesenteric bed. The lipoxygenase metabolites are likely to be formed in the vascular endothelium, whereas the COX metabolite, which could be PGF2alpha, is apparently formed within the vascular smooth muscle.

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Section: Discussionmentioning

confidence: 86%

Effects of eicosanoids and nitric oxide on the noradrenaline‐induced contractions in the rat mesenteric bed

Peredo

Adler‐Graschinsky

2000

J. Autonom. Pharmacol.

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“…Cleavage of membrane lipids by PLA 2 causes the release of arachidonic acid that can be metabolized via the cyclo‐oxygenase and TXA 2 synthase enzymes into TXA 2 ( Mentha & Roberts, 1983 ). TXA 2 is produced mainly by the media layer of intact blood vessels ( Brunkwall et al ., 1987 ), although some is synthesized by vascular endothelial cells ( Ingermam‐Wojenski et al ., 1981 ). The contractions induced by myricetin were inhibited either in the presence of the phospholipase A 2 inhibitor, quinacrine, or the cyclo‐oxygenase inhibitor, indomethacin.…”

Section: Discussionmentioning

confidence: 99%

Involvement of thromboxane A₂ in the endothelium‐dependent contractions induced by myricetin in rat isolated aorta

Jiménez

Andriambeloson

Duarte

et al. 1999

British J Pharmacology

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1 The present study was undertaken to analyse the mechanism of the contractile response induced by the bio¯avonoid myricetin in isolated rat aortic rings. 2 Myricetin induced endothelium-dependent contractile responses (maximal value=21+2% of the response induced by 80 mM KCl and pD 2 =5.12+0.03). This e ect developed slowly, reached a peak within 6 min and then declined progressively. 3 Myricetin-induced contractions were almost abolished by the phospholipase A 2 (PLA 2 ) inhibitor, quinacrine (10 mM), the cyclo-oxygenase inhibitor, indomethacin (10 mM), the thromboxane synthase inhibitor, dazoxiben (100 mM), the putative thromboxane A 2 (TXA 2 )/prostaglandin endoperoxide receptor antagonist, ifetroban (3 mM). These contractions were abolished in Ca 2+ -free medium but were not a ected by the Ca 2+ channel blocker verapamil (10 mM). 4 In cultured bovine endothelial cells (BAEC), myricetin (50 mM) produced an increase in cytosolic free calcium ([Ca 2+ ] i ) which peaked within 1 min and remained sustained for 6 min, as determined by the¯uorescent probe fura 2. This rise in [Ca 2+ ] i was abolished after removal of extracellular Ca 2+ in the medium. 5 Myricetin (50 mM) signi®cantly increased TXB 2 production both in aortic rings with and without endothelium and in BAEC. These increases were abolished both by Ca 2+ -free media and by indomethacin. 6 Taken together, these results suggests that myricetin stimulates Ca 2+ in¯ux and subsequently triggers the activation of the PLA 2 and cyclo-oxygenase pathways releasing TXA 2 from the endothelium to contract rat aortic rings. The latter response occurs via the activation of T p receptors on vascular smooth muscle cells.

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Prostaglandins

Schröder¹,

Gryglewski²,

Mehta³

et al. 1990

Pharmacology of Antihypertensive Therapeutics

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Prostacyclin and thromboxane release from the vessel wall — Comparison between an incubation and a perfusion model

Cited by 13 publications

References 22 publications

Effects of eicosanoids and nitric oxide on the noradrenaline‐induced contractions in the rat mesenteric bed

Effects of eicosanoids and nitric oxide on the noradrenaline‐induced contractions in the rat mesenteric bed

Involvement of thromboxane A₂ in the endothelium‐dependent contractions induced by myricetin in rat isolated aorta

Prostaglandins

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Prostacyclin and thromboxane release from the vessel wall — Comparison between an incubation and a perfusion model

Cited by 13 publications

References 22 publications

Effects of eicosanoids and nitric oxide on the noradrenaline‐induced contractions in the rat mesenteric bed

Effects of eicosanoids and nitric oxide on the noradrenaline‐induced contractions in the rat mesenteric bed

Involvement of thromboxane A2 in the endothelium‐dependent contractions induced by myricetin in rat isolated aorta

Prostaglandins

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Involvement of thromboxane A₂ in the endothelium‐dependent contractions induced by myricetin in rat isolated aorta