The effects of ecdysterone and enalapril on nitric oxide synthesis and the markers of oxidative stress in streptozotocin-induced diabetes in rats: a comparative study.

Cardiovascular functions in diabetes greatly depend on constitutive NOS (cNOS) activity. A comparative study of the effects of a steroid hormone ecdysterone and enalapril, an ACE inhibitor widely used to treat cardiac disorders on cNOS, inducible NOS (iNOS), xanthine oxidoreductase (XOR) activity, RNS, ROS, and lipid peroxidation in heart tissue in experimental diabetes was conducted. The rat model of diabetes was established by streptozotocin injection.

Pyridoxal-5-phosphate induced cardioprotection in aging associated with up-expression of cystathionine-γ-lyase, 3-mercaptopyruvate sulfurtransferase, and ATP-sensitive potassium channels.

Background: In the present work, we investigated the cardioprotective potential of pyridoxal-5-phosphate (PLP) in old rats as a cofactor of enzymes that synthesize hydrogen sulphide (H S).

Materials And Methods: PLP was administered per os in a dose of 0.7 mg per kg daily for 2 weeks.

H S donor improves heart function and vascular relaxation in diabetes.

Background And Aims: Diabetes dramatically increases the risk of cardiovascular complications and mortality. Hydrogen sulphide plays an important role in reducing oxidative stress. Several studies demonstrated that hydrogen sulphide protects islet beta cells from oxidant stress damage and decreases apoptosis.

Diazoxide affects mitochondrial bioenergetics by the opening of mKATP channel on submicromolar scale.

Background: Cytoprotection afforded by mitochondrial ATP-sensitive K-channel (mK-channel) opener diazoxide (DZ) largely depends on the activation of potassium cycle with eventual modulation of mitochondrial functions and ROS production. However, generally these effects were studied in the presence of Mg∙ATP known to block K transport. Thus, the purpose of our work was the estimation of DZ effects on K transport, K cycle and ROS production in rat liver mitochondria in the absence of Mg∙ATP.

GPR55 agonist lysophosphatidylinositol and lysophosphatidylcholine inhibit endothelial cell hyperpolarization via GPR-independent suppression of Na-Ca exchanger and endoplasmic reticulum Ca refilling.

Lysophosphatidylinositol (LPI) and lysophosphatidylcholine (LPC) are lipid signaling molecules that induce endothelium-dependent vasodilation. In addition, LPC suppresses acetylcholine (Ach)-induced responses. We aimed to determine the influence of LPC and LPI on hyperpolarizing responses in vitro and in situ endothelial cells (EC) and identify the underlying mechanisms.

The Effect Of NO Donor on Calcium Uptake and Reactive Nitrogen Species Production in Mitochondria.

Background/aims: NO and reactive nitrogen species (RNS) are thought to be physiologically important effectors of mitochondrial calcium transport, but this issue was not studied in a living organism. According to literature, the modulation of Ca2+ uptake could influence RNS production via the action on mitochondrial NO synthase (mtNOS). The aim of this work was to study the effect of in vivo administration of NO donor nitroglycerine (NG) on matrix Ca2+ accumulation, RNS production and mtNOS activity.

The effect of atp-dependent potassium uptake on mitochondrial functions under acute hypoxia.

The opening of mitochondrial K(+) АТР-channel (mtK(+) АТР-channel) is supposed to be important in the modulation of mitochondrial functions under hypoxia, but the underlying mechanisms have not been clarified yet. The aim of this work was to study the effect of acute hypoxia on mtK(+) АТР-channel activity and to estimate the contribution of the channel in the modulation of mitochondrial functions. MtK(+) АТР-channel activity was assessed polarographically from the rate of State 4 respiration and by potentiometric monitoring of potassium efflux from deenergized mitochondria.

N-Arachidonoyl glycine suppresses Na⁺/Ca²⁺ exchanger-mediated Ca²⁺ entry into endothelial cells and activates BK(Ca) channels independently of GPCRs.

Background And Purpose: N-Arachidonoyl glycine (NAGly) is a lipoamino acid with vasorelaxant properties. We aimed to explore the mechanisms of NAGly's action on unstimulated and agonist-stimulated endothelial cells.

Experimental Approach: The effects of NAGly on endothelial electrical signalling were studied in combination with vascular reactivity.

Reduced hyperpolarization of endothelial cells following high dietary Na+: effects of enalapril and tempol.

1. High dietary Na(+) is associated with impaired vascular endothelial function. However, the underlying mechanisms are not completely understood.

Purine release: a protective signaling mechanism of the mitochondrial permeability transition pore in ischemia.

Both mitochondrial permeability transition pore (PTP) opening and purine signaling are implicated in cardioprotection via ischemic preconditioning (IPC). The PTP opening is accomponied by release ofintramitochondrial solutes, and therefore we hypothesized that purine release from mitochondria during PTP opening may by required for IPC signaling. Herein we show that upon PTP opening, isolated mitochondria release adenosine, inosine and 3'-ribosyl uric acid monophosphate (3-RUAMP), and that perfused hearts subject to IPC release inosine and 3-RUAMP derivatives.

Endothelial dysfunction: Possible mechanisms and ways of correction.

Background: Endothelial function is impaired in atherosclerosis, hypertension, diabetes and aging, and this may be associated with an attenuated ability of endothelial cells to generate nitric oxide (NO).

Objectives: To evaluate possible alterations in endothelium-dependent relaxation in rat aortic rings, the activity of constitutive NO synthase and endothelial electrical responses to acetylcholine (Ach) in rat aorta, and the effect of one month of treatment with the angiotensin-converting enzyme inhibitor enalapril on endothelial function.

Methods: Endothelial membrane potential was measured in excised rat aorta using the perforated patch-clamp technique.

The water-soluble vitamin E analogue Trolox protects against ischaemia/reperfusion damage in vitro and ex vivo. A comparison with vitamin E.

We investigated the activities, both in vitro and ex vivo, of the water-soluble vitamin analogue Trolox in a model of isolated heart ischaemia-reperfusion and we compared them with those of alpha -tocopherol. Isolated rat hearts were perfused with Krebs-Henseleit solution. For in vitro experiments, the hearts were perfused with Trolox (20 micromol l (-1)) and were subsequently subjected to 20 min of global ischaemia and 40 min of post-ischaemic reperfusion.