Time-course of the alterations in prostanoid production and in contractile responses of mesenteric beds isolated from streptozotocin diabetic rats

Peredo, Horacio A.; Feleder, Ethel; Adler‐Graschinsky, Edda

doi:10.1054/plef.1999.0035

Cited by 14 publications

(14 citation statements)

References 16 publications

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“…These data show that in diabetic animals phenylephrine is unable to release vasoconstrictive prostanoids from MVB smooth muscle and that this is the major mechanism explaining the difference in reactivity to this agent observed in diabetic rats. Using noradrenaline with an agonist, Peredo et al, 1999, Peredo, 2001 obtained similar data for rats with diabetes mellitus in two distinct models (STZ diabetic rats and rats with diabetes similar to the human type II). However, 8 weeks after STZ induction of diabetes, the vasoconstrictive effect of noradrenaline was again reduced by indomethacin perfusion.…”

Section: Discussionmentioning

confidence: 83%

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Effects of prostanoids on phenylephrine-induced contractions in the mesenteric vascular bed of rats with streptozotocin-induced diabetes mellitus

Leone

Coelho

2004

Life Sciences

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Section: Discussionmentioning

confidence: 83%

“…Changes in arachidonic acid metabolism have been reported to occur in diabetic animals (Peredo et al, 1999). However it is not known if these changes occur in the endothelium or in the vascular smooth muscle in this model.…”

Section: Introductionmentioning

confidence: 72%

Effects of prostanoids on phenylephrine-induced contractions in the mesenteric vascular bed of rats with streptozotocin-induced diabetes mellitus

Leone

Coelho

2004

Life Sciences

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“…In diabetic rats, a decrease of prostacyclin and PGE 2 synthesis was reported in the aorta and mesenteric vascular bed [11,12]. Previous studies indicate that the levels of these prostaglandins remain unchanged in the coronary vessels of diabetic rats [13], while increased prostacyclin production has been shown in diabetic mice aorta [9].…”

Section: Discussionmentioning

confidence: 97%

Inhibition of cyclooxygenase-2 causes a decrease in coronary flow in diabetic mice. The possible role of PGE2 and dysfunctional vasodilation mediated by prostacyclin receptor

et al. 2015

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Several lines of evidence suggest that cyclooxygenase-2 (COX-2) activity can have a beneficial role in the maintenance of vascular tone of the blood vessels in diabetes. Specifically, the increased production of prostacyclin (PGI2) and prostaglandin E2 (PGE2), mediated by COX-2, has been suggested to compensate for decreased synthesis of nitric oxide (NO). The study investigates whether inhibition of COX-2 may reduce the coronary flow in diabetic animals and may also lead to decreased synthesis of prostaglandins. Mice aged 18-20 weeks were used for the study: those with leptin receptor deficiency (db/db) served as a model of diabetes while heterozygous (db/+) mice served as controls. Coronary flow was measured by the Langendorff method, and prostaglandin synthesis by myocardia was assayed in heart perfusates. COX-2 inhibition was found to reduce basal coronary flow in db/db mice but had no effect in db/+ mice. Secretion of PGE2 was found to be higher in db/db mice, while prostacyclin synthesis did not differ. COX-2 inhibition decreased production of both prostaglandins to similar levels in both groups. The use of ONO-1301, a specific agonist for the prostacyclin receptor revealed that vasodilating responses mediated by the receptor were impaired in db/db mice. The expression levels of the receptor in cardiac tissue did not differ between the groups. It is concluded that the increased COX-2 contribution to vasodilation in diabetic animals appears to be partially a result of increased COX-2-dependent synthesis of PGE2 and also may be caused by impaired vasodilation mediated by the prostacyclin receptor.

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“…Indeed, the decreased relaxation of pial arterioles of diabetic rats in vivo [1] and of diabetic isolated resistance arteries [2] and aortas [3] is restored by nonspecific cyclooxygenase blockade and by prostanoid receptor antagonists. Changes in the metabolism of arachidonic acid have also been reported in diabetic males, such as an increased production of thromboxane B 2 (TXB 2 ) in rabbit aortas [3] and an increased release of TXB 2 and prostaglandin F 2 α (PGF 2 α ) in the rat mesenteric bed [4]. …”

Section: Introductionmentioning

confidence: 99%

Decreased Endothelium-Dependent Vasodilation in Diabetic Female Rats: Role of Prostanoids

Akamine

Urakawa²,

Oliveira³

et al. 2006

J Vasc Res

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Overproduction of vasoconstrictor prostanoids and reduced prostacyclin levels have been related to the male diabetic-linked vascular dysfunction. However, it is not clear yet if these changes also occur in diabetic females. The aim of this study was to verify the role of prostanoids in the vascular dysfunction of diabetic female rats. The parameters studied were the mesenteric arteriolar reactivity (intravital microscopy and isolated perfused arteriolar bed), prostanoid measurement (enzyme immunoassay), superoxide generation (intravital fluorescence microscopy), and the presence of peroxynitrite (Western blot for nitrotyrosine-containing proteins). The response to acetylcholine was decreased in arterioles of diabetic female rats and diclofenac, but not ridogrel, corrected the altered response. The unstimulated (basal) release of thromboxane B₂ (TXB₂), but not prostaglandin F₂_α (PGF₂_α) or 6-keto-PGF₁_α, was increased in the mesenteric perfusate from diabetic female rats. Increased production of PGF₂_α and 6-keto-PGF₁_α, but not TXB₂, was induced by acetylcholine in diabetic arterioles. The superoxide generation was increased in diabetic female rats and diclofenac corrected it. Diabetes increased nitrotyrosine-containing proteins in mesenteric microvessels. In conclusion, our data show that the increase of constrictor prostanoid release, most likely PGF₂_α, could be involved in the reduced endothelium-dependent vasodilation of diabetic female rats. In addition, the enhanced activation of cyclooxygenase may be a source of superoxide anion generation in this model.

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Time-course of the alterations in prostanoid production and in contractile responses of mesenteric beds isolated from streptozotocin diabetic rats

Cited by 14 publications

References 16 publications

Effects of prostanoids on phenylephrine-induced contractions in the mesenteric vascular bed of rats with streptozotocin-induced diabetes mellitus

Effects of prostanoids on phenylephrine-induced contractions in the mesenteric vascular bed of rats with streptozotocin-induced diabetes mellitus

Inhibition of cyclooxygenase-2 causes a decrease in coronary flow in diabetic mice. The possible role of PGE2 and dysfunctional vasodilation mediated by prostacyclin receptor

Decreased Endothelium-Dependent Vasodilation in Diabetic Female Rats: Role of Prostanoids

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