Effect of angiotensin II and norepinephrine on release of prostaglandins E2 and I2 by the perfused rat mesenteric artery

Desjardins-Giasson, Suzanne; Gutkowska, Jolanta; García, Raúl; Genest, Jacques

doi:10.1016/0090-6980(82)90182-4

Cited by 36 publications

(8 citation statements)

References 10 publications

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“…These aortic rings devoted to PG measurement were not subjected to passive tension. Although flow and dynamic changes such as acute stretch or pulsatile flow evoke the release of PGs (4,5,32), in steady-state conditions and in the absence of flow the level of stretch or the level of transluminal pressure, per se, do not appear to affect PG release (4,5,7,9). The equilibration time was 1 h, during which the solution was changed every 15 min.…”

Section: Methodsmentioning

confidence: 99%

In SHR aorta, calcium ionophore A-23187 releases prostacyclin and thromboxane A₂ as endothelium-derived contracting factors

Gluais¹,

Paysant²,

Badier‐Commander³

et al. 2006

American Journal of Physiology-Heart and Circulatory Physiology

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In mature spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY), acetylcholine and the calcium ionophore A-23187 release endothelium-derived contracting factors (EDCFs), cyclooxygenase derivatives that activate thromboxane-endoperoxide (TP) receptors on vascular smooth muscle. The EDCFs released by acetylcholine are most likely prostacyclin and prostaglandin (PG)H(2), whereas those released by A-23187 remain to be identified. Isometric tension and the release of PGs were measured in rings of isolated aortas of WKY and SHR. A-23187 evoked the endothelium-dependent release of prostacyclin, thromboxane A(2), PGF(2alpha), PGE(2), and possibly PGH(2) (PGI(2) >> thromboxane A(2) = PGF(2alpha) = PGE(2)). In SHR aortas, the release of prostacyclin and thromboxane A(2) was significantly larger in response to A-23187 than to acetylcholine. In response to the calcium ionophore, the release of thromboxane A(2) was significantly larger in aortas of SHR than in those of WKY. In both strains of rat, the inhibition of cyclooxygenase-1 prevented the release of PGs and the occurrence of endothelium-dependent contractions. Dazoxiben, the thromboxane synthase inhibitor, abolished the A-23187-dependent production of thromboxane A(2) and inhibited by approximately one-half the endothelium-dependent contractions. U-51605, an inhibitor of PGI synthase, reduced the release of prostacyclin elicited by A-23187 but induced a parallel increase in the production of PGE(2) and PGF(2alpha), suggestive of a PGH(2) spillover, which was associated with the enhancement of the endothelium-dependent contractions. These results indicate that in the aorta of SHR and WKY, the endothelium-dependent contractions elicited by A-23187 involve the release of thromboxane A(2) and prostacyclin with a most likely concomitant contribution of PGH(2).

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Section: Methodsmentioning

confidence: 99%

In SHR aorta, calcium ionophore A-23187 releases prostacyclin and thromboxane A₂ as endothelium-derived contracting factors

Gluais¹,

Paysant²,

Badier‐Commander³

et al. 2006

American Journal of Physiology-Heart and Circulatory Physiology

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“…Second, the endothelial cells may produce more vasodilator substances after neo-intima formation. Evidence exists that angiotensin II can stimulate the release of dilator prostaglandins (Desjardins-Giasson et al, 1982) and that angiotensin II-induced endothelium-dependent relaxations of canine renal arteries may be mediated by release of cyclo-oxygenase products from the endothelium (Toda, 1984). Another possible mediator of the decreased sensitivity to angiotensin II is endothelium-derived NO.…”

Section: Angiotensinmentioning

confidence: 99%

Vasoconstrictor responses after neo‐intima formation and endothelial removal in the rabbit carotid artery

Meyer¹,

Bult

Üstünes

et al. 1994

British J Pharmacology

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1 The present study examined the responses of the rabbit carotid artery to five vasoconstrictors after neo-intima formation induced by perivascular collar treatment and evaluated the role of constitutive and inducible nitric oxide (NO) synthase and endothelial cells (ECs). 2 Ring segments of the rabbit carotid artery were mounted in organ chambers for isometric tension recording. Neo-intima-bearing vessels developed less force (Em,.) in response to KCl, the thromboxanemimetic U-46619 and 5-hydroxytryptamine (5-HT), but not to angiotensin I and II. 3 The collar-treatment increased the sensitivity to 5-HT, and decreased the sensitivity to angiotensin II. The sensitivity to U-46619 and angiotensin I remained unchanged. 4 Mechanical removal of ECs and inhibition of NO biosynthesis by N0-monomethyl-L-arginine (L-NMMA) and N0-nitro-L-arginine (L-NOARG) increased the sensitivity to 5-HT in sham and collartreated segments to the same extent. The effects of collar-treatment and endothelial removal or treatment with inhibitors of NO biosynthesis were additive. Inhibition of NO biosynthesis failed to augment sensitivity to 5-HT after endothelial denudation. L-NOARG increased the force development to KC1 in sham and collar-treated segments to the same extent. However, L-NMMA and L-NOARG failed to augment the contractile responses of neo-intima-bearing vessels to 5-HT and KCl after endothelial removal. 5 The responses to angiotensin I were not altered, either by the neo-intima or by endothelial removal. In arteries with a neo-intima the sensitivity to angiotensin II was decreased. Removal of the endothelium or incubation with L-NOARG counteracted this rightward shift and increased Em|. 6 Our results demonstrate that contractions to 5-HT, angiotensin II and KCl are modulated by NO in both sham and neo-intima-bearing vessels. Inhibition of NO biosynthesis and collar treatment resulted in additive effects on the EC50 values, suggesting that the 5-HT and angiotension (AT) receptors on the smooth muscle cells are also modified by the formation of a neo-intima. Furthermore, the reduced contractile responses of segments with a neo-intima are not due to NO formed by an inducible NO synthase in those vessels.

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“…The vasoconstrictor action of PGs released by the peptide may be balanced by the action of vasodilator PGs, such as PGI2, or ANG II may not release PGs from these blood vessels in amounts eliciting significant responses. Many studies reported so far indicate the release of PGs from a vari ety of blood vessels from different mammals in response to ANG II (6,(21)(22)(23)(24); therefore, the latter alternative is less likely. Figure 4 summarizes the effect of indomethacin on the ANG II-induced contraction in various blood vessels from monkeys, obtained in the present and previous (14) studies.…”

Section: Discussionmentioning

confidence: 99%

Different Modulation by Cyclooxygenase Inhibitors of the Response to Angiotensin II in Monkey Arteries and Veins.

Yoshida

Yamazaki²,

Toda³

1991

Jpn.J.Pharmacol

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ABSTRACT-In coronary, renal and femoral arteries and mesenteric veins isolated from Japanese monkeys, tachyphylaxis to angiotensin (ANG) II (107 M)-induced contraction rapidly developed. Contractions caused by ANG II in coronary arteries were attenuated by treatment with indomethacin and aspirin and also by endothelium denudation. Indomethacin inhibited the response of the arteries with and without endo thelium to a similar extent. OKY 046, a thromboxane A2 synthesis inhibitor, failed to inhibit the response. In contrast, contractions of renal arteries were potentiated and prolonged by the cyclooxygenase inhibitors. ANG II-induced contractions of mesenteric veins were prolonged but those of femoral arteries were not altered by in domethacin. It is concluded that ANG II contracts monkey coronary arteries, possibly due to the release of vasoconstrictor prostanoids but not thromboxane A2 from endothelial and subendothelial tissues and also due to its direct action on smooth mus cle, whereas contractions of renal arteries and mesenteric veins are blunted by vaso dilator prostanoids, possibly PGI2. Cylooxygenase products even if released do not appear to regulate femoral artery contractions produced by ANG II.

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Effect of angiotensin II and norepinephrine on release of prostaglandins E2 and I2 by the perfused rat mesenteric artery

Cited by 36 publications

References 10 publications

In SHR aorta, calcium ionophore A-23187 releases prostacyclin and thromboxane A₂ as endothelium-derived contracting factors

In SHR aorta, calcium ionophore A-23187 releases prostacyclin and thromboxane A₂ as endothelium-derived contracting factors

Vasoconstrictor responses after neo‐intima formation and endothelial removal in the rabbit carotid artery

Different Modulation by Cyclooxygenase Inhibitors of the Response to Angiotensin II in Monkey Arteries and Veins.

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Effect of angiotensin II and norepinephrine on release of prostaglandins E2 and I2 by the perfused rat mesenteric artery

Cited by 36 publications

References 10 publications

In SHR aorta, calcium ionophore A-23187 releases prostacyclin and thromboxane A2 as endothelium-derived contracting factors

In SHR aorta, calcium ionophore A-23187 releases prostacyclin and thromboxane A2 as endothelium-derived contracting factors

Vasoconstrictor responses after neo‐intima formation and endothelial removal in the rabbit carotid artery

Different Modulation by Cyclooxygenase Inhibitors of the Response to Angiotensin II in Monkey Arteries and Veins.

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In SHR aorta, calcium ionophore A-23187 releases prostacyclin and thromboxane A₂ as endothelium-derived contracting factors

In SHR aorta, calcium ionophore A-23187 releases prostacyclin and thromboxane A₂ as endothelium-derived contracting factors