Glycyrrhetinic acid reverses the lipopolysaccharide-induced hypocontractility to noradrenaline in rat aorta: implications to septic shock.

Septic shock and associated vascular hyporeactivity to vasoconstrictor agonists remain a major problem of critical care medicine. Here we report that glycyrrhetinic acid (GA), the active component of licorice, effectively restores vascular contractility in the model of lipopolysaccharide (LPS)-treated rat aorta. GA was as effective as the NO synthase inhibitor N(G)-nitroarginine methylester.

[Dietary flavonoids and human health].

Due to antioxidant properties linked to their polyphenolic structure, dietary flavonoids are supposed to protect the organism against deleterious effects of environmental oxidants. Indeed prospective epidemiologic studies on cohorts have shown inverse correlations between consumption of some foods or beverages with high flavonoid content, (especially flavanols and anthocyanins), and coronary stroke mortality or prevalence of neurodegenerative diseases including Alzheimer's and Parkinson's diseases. These include red wine, some grape juices, red fruits, tea and cocoa, The hypothesis of cause effect relationship between dietary flavonoid intake and observed protection is further supported by several short term controlled randomised clinical trials.

Y27632, a Rho-activated kinase inhibitor, normalizes dysregulation in alpha1-adrenergic receptor-induced contraction of Lyon hypertensive rat artery smooth muscle.

RhoA-activated kinase (ROK) is involved in the disorders of smooth muscle contraction found in hypertension model animals and patients. We examined whether the alpha1-adrenergic receptor agonist-induced ROK signal is perturbed in resistance small mesentery artery (SMA) of Lyon genetically hypertensive (LH) rats, using a ROK antagonist, Y27632. Smooth muscle strips of SMA and aorta were isolated from LH and Lyon normotensive (LN) rats.

Targeted and persistent effects of NO mediated by S-nitrosation of tissue thiols in arteries with endothelial dysfunction.

We have previously demonstrated that in endothelium-denuded arteries, S-nitrosation of cysteine residues is a mechanism of formation of releasable nitric oxide (NO) stores, accounting for the long-lasting relaxation induced by S-nitrosating agents like S-nitrosoglutathione (GSNO). Here, we have investigated whether such effects could also be obtained in arteries exhibiting oxidative stress-associated endothelial dysfunction. Rats were implanted or not with a minipump delivering saline or angiotensin II for 14 days.