Vascular responsiveness in young, diabetic, and aging hyperinsulinemic rats

Félétou, Michel; Moreau, Nathalie; Duhault, J

doi:10.1016/0024-3205(94)90119-8

Cited by 12 publications

(9 citation statements)

References 18 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Makino, K. Kamata: Vasoconstriction in diabetic state 1414 Systolic blood pressure, as recorded using the talecuff technique, was lower in diabetic rats than in the control rats. This result is in agreement with a previous report [23], but there are also reports claiming an enhancement [24] or no change [25±26] in blood pressure. The lower blood pressure in diabetic rats may be due to a cardiac dysfunction or to a decreased contractility of resistance vessels, such as those of the mesenteric arterial bed, or both.…”

Section: Discussionsupporting

confidence: 93%

Possible modulation by endothelin-1, nitric oxide, prostaglandin I 2 and thromboxane A 2 of vasoconstriction induced by an α-agonist in mesenteric arterial bed from diabetic rats

Kamata

1998

Diabetologia

View full text Add to dashboard Cite

Diabetes mellitus is associated with vascular complications, including an impairment of vascular function and alterations in the reactivity of blood vessels to neurotransmitters in the macro-and microvasculature. The effect of diabetes on vascular morphology and function has been studied using a wide variety of Diabetologia (1998) 41: 1410±1418 OriginalsPossible modulation by endothelin-1, nitric oxide, prostaglandin I 2 and thromboxane A 2 of vasoconstriction induced by an a-agonist in mesenteric arterial bed from diabetic rats

show abstract

Section: Discussionsupporting

confidence: 93%

Possible modulation by endothelin-1, nitric oxide, prostaglandin I 2 and thromboxane A 2 of vasoconstriction induced by an α-agonist in mesenteric arterial bed from diabetic rats

Kamata

1998

Diabetologia

View full text Add to dashboard Cite

show abstract

“…Conflicting results have been recorded on the altered PE or 5-HT contractility in STZ-induced diabetic vessels indicating either an increased [40,41], decreased [42,43] or unaltered reactivity [44,45]. Both PE and 5-HT stimulate phospholipase C on vascular smooth muscle cell membrane via activation of · 1 -adrenoceptors and 5-HT 2/1c receptors, respectively, resulting in phosphoinositide hydrolysis with a subsequent increase in cytosolic calcium content and the activation of diacylglycerol-protein kinase C pathway [46].…”

Section: Discussionmentioning

confidence: 98%

Effect of Dietary Vitamin E Supplementationon Vascular Reactivity of Thoracic Aorta in Streptozotocin-Diabetic Rats

Çınar¹,

Ülker²,

Alper

et al. 2001

Pharmacology

View full text Add to dashboard Cite

The present study evaluated the effect of dietary vitamin E supplementation (1,000 mg/kg chow) on the alterations in vascular reactivity of streptozotocin-diabetic aorta of Wistar rats. After 12 weeks of treatment, thoracic aortic rings of rats were mounted in organ baths and contractile responses to phenylephrine and 5-hydroxytryptamine and relaxant responses to acetylcholine, calcium ionophore and sodium nitroprusside were assessed. Plasma vitamin E concentration as measured by HPLC was markedly decreased in diabetic rats and increased with dietary vitamin E supplementation. Induction of diabetes significantly impaired endothelium-dependent relaxations to acetylcholine and calcium ionophore in aortic rings, but did not change endothelium-independent relaxation to sodium nitroprusside. Vitamin E significantly improved the impaired endothelium-dependent relaxations, further it decreased the enhanced contractile response to phenylephrine and 5-hydroxytryptamine in diabetic rings. The mechanical denudation of endothelium or the chemical inhibition of endothelium-dependent relaxation with N^ω-nitro-L-arginine methyl ester (100 µmol/l) significantly increased phenylephrine contractility in control rings and the rings of diabetic rats treated with vitamin E; such a difference was not observed in diabetic rats fed with normal diet. Liver and lung malondialdehyde concentrations, as an index of lipid peroxidation, were increased in diabetic rats and significantly decreased with vitamin E supplementation. It is concluded that dietary supplementation of vitamin E improved endothelial dysfunction in insulin-dependent model of uncontrolled diabetes, probably decreasing membranal lipid peroxidation.

show abstract

“…Other ␣-2 AR agonists also have been shown to stimulate NO synthesis in endothelial cell cultures (41) and to stimulate NO-dependent vasodilation in animals (28). However, L-arginine targeting receptor(s) other than ␣-2 AR cannot be discounted, because rauwolscine is also known to act on serotonin [5-hydroxytryptamine (5-HT)] receptors (42,43).…”

Section: Discussionmentioning

confidence: 99%

Receptor-mediated activation of nitric oxide synthesis by arginine in endothelial cells

Joshi¹,

Ferguson²,

Johnson

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

Arginine contains the guanidinium group and thus has structural similarity to ligands of imidazoline and ␣-2 adrenoceptors (␣-2 AR). Therefore, we investigated the possibility that exogenous arginine may act as a ligand for these receptors in human umbilical vein endothelial cells and activate intracellular nitric oxide (NO) synthesis. Idazoxan, a mixed antagonist of imidazoline and ␣-2 adrenoceptors, partly inhibited L-arginine-initiated NO formation as measured by a Griess reaction. Rauwolscine, a highly specific antagonist of ␣-2 AR, at very low concentrations completely inhibited NO formation. Like L-arginine, agmatine (decarboxylated arginine) also activated NO synthesis, however, at much lower concentrations. We found that dexmedetomidine, a specific agonist of ␣-2 AR was very potent in activating cellular NO, thus indicating a possible role for ␣-2 AR in L-arginine-mediated NO synthesis. D-arginine also activated NO production and could be inhibited by imidazoline and ␣-2 AR antagonists, thus indicating nonsubstrate actions of arginine. Pertussis toxin, an inhibitor of G proteins, attenuated L-arginine-mediated NO synthesis, thus indicating mediation via G proteins. L-type Ca 2؉ channel blocker nifedipine and phospholipase C inhibitor U73122 inhibited NO formation and thus implicated participation of a second messenger pathway. Finally, in isolated rat gracilis vessels, rauwolscine completely inhibited the L-arginine-initiated vessel relaxation. Taken together, these data provide evidence for binding of arginine to membrane receptor(s), leading to the activation of endothelial NO synthase (eNOS) NO production through a second messenger pathway. These findings provide a previously unrecognized mechanistic explanation for the beneficial effects of L-arginine in the cardiovascular system and thus provide new potential avenues for therapeutic development. agmatine ͉ rauwolscine ͉ calcium A rginine is critical to normal growth and multiple physiological processes. It serves as a precursor for the synthesis not only of proteins but also of NO, urea, polyamines, and agmatine. The unequivocal demonstration that NO is the product of NO synthase (NOS)-catalyzed oxidation of L-arginine led to widespread interest in the actions of L-arginine. The K m of L-arginine for endothelial NOS (eNOS) is determined to be 2.9 M (1), and the intracellular L-arginine concentrations are in the range of 0.8-2.0 mM. In other words, cells maintain saturating levels of L-arginine as a substrate for NO synthases. However, an external supply of L-arginine is still required for the cellular production of NO (2). This requirement of exogenous arginine for the cellular NO production is termed ''arginine paradox.'' A number of mechanisms have been proposed to address this phenomenon, including endogenous NOS inhibitors and compartmentalization of intracellular L-arginine. Some have proposed that endogenous NOS inhibitors [e.g., asymmetric dimethylarginine (ADMA)] modulate NO levels by antagonizing intracellular L-arginine (3). An alternative...

show abstract

Vascular responsiveness in young, diabetic, and aging hyperinsulinemic rats

Cited by 12 publications

References 18 publications

Possible modulation by endothelin-1, nitric oxide, prostaglandin I 2 and thromboxane A 2 of vasoconstriction induced by an α-agonist in mesenteric arterial bed from diabetic rats

Possible modulation by endothelin-1, nitric oxide, prostaglandin I 2 and thromboxane A 2 of vasoconstriction induced by an α-agonist in mesenteric arterial bed from diabetic rats

Effect of Dietary Vitamin E Supplementationon Vascular Reactivity of Thoracic Aorta in Streptozotocin-Diabetic Rats

Receptor-mediated activation of nitric oxide synthesis by arginine in endothelial cells

Contact Info

Product

Resources

About