Biomedical subjects

Simona Mihaela Slătineanu

Publications and source records attributed to Simona Mihaela Slătineanu.

8 recordsLinked to original sources

PubMed2004

New bioactive angiotensins formation pathways and functional involvements.

After a brief review of the actual knowledge concerning the circulating and tissue Renin-Angiotensin System (RAS) as a unitary hormonal system, the cognitive acquisitions regarding the formation and action mechanisms of the new biologically active angiotensins will be presented. The review of the enzymatic pathways for their synthesis and inactivation, as metabolism products of angiotensin II (1-8), will be followed by the presentation of the main physio-pharmacological actions of angiotensin III (2-8), angiotensin IV (3-8) and angiotensin (1-7). The functional involvements of the cerebral angiotensin IV in what concerns its possible participation in the normal neurochemical processes of memory and in the neurodegenerative processes of Alzheimer disease will be exposed, together with the vasodilating effects of angiotensin (1-7) as counteracting factor for the constricting effects of angiotensin II. The data concerning the bioactive fragments of angiotensin II will be accompanied by those regarding its implication in the cardiovascular modeling and the induction of oxidative stress, inflammation, atherogenesis, etc. In their turn, personal researches bring new experimental evidences in favor of interactions between angiotensin (1-7) and angiotensin II within the rat thoracic aorta. Biphasic, dose-dependent effects were observed for angiotensin (1-7), induced both through nitric oxide, kinins and prostaglandin release for counteracting the vasoconstricting effects of angiotensin II and the modulation of its own vasodilator action.

Angiotensins↗

PubMedDate not supplied

[Effects of polyamine-loaded liposomes on liver mitochondrial permeability transition].

The objective of the present study was represented by the effects of polyamineloaded liposomes on hepatic mitochondrial permeability transition (MPT). MPT was appreciated through the swelling of the isolated guinea-pig liver mithocondria induced by Ca2+, at 540 nm, using a diode-array 8452 UV-VIS spectrophotometer and a General Purpose software (Hewlett-Packard). Polyamines encapsulated in liposomes might inhibit the appearance of MPT induced by Ca2+, directly proportional to electrical charge: spermine > spermidine > putrescine > cadaverine. Thus, together with some previous data, it was observed that spermine may modulate hepatic MPT from the exterior, as well as from the interior of mitochondria. Moreover, spermidine and putrescine may also modulate MPT from the interior of mitochondria at low doses, and from the exterior only at high doses. The changes in mitochondrial membranes lipid composition (as done by control liposomes) are slightly influencing the MPT. The increase in membrane rigidity through the use of 40% cholesterol-enriched liposomes is drastically decreasing the appearance and development of MPT.

Animals↗

PubMedDate not supplied

[Cytosolic calcium dynamics and smooth muscle contraction.III Plasmalemmal calcium fluxes].

Smooth muscle contractile activity depends upon cytosolic Ca2+, the Ca(2+)-sensitivity of actin-myosin interaction and several auxiliary mechanisms. This section presents the plasmalemmal Ca2+ fluxes in relation with the functional structure of their supportive proteins and the contractile impact. Summaries of classical data are accompanied by examples of recent advances. Ca2+ influx occurs mainly via the L and T types of voltage-operated Ca2+ channels, the store-operated Ca2+ channels and the non-selective cation channels (operated by membrane receptors or mechanical stimuli). The plasmalemmal Ca2+ ATPase and Na/Ca antiport function to limit increases in cytosolic Ca2+; Na/Ca effect is opposite when driven to operate in the reverse mode.

Calcium↗

PubMedDate not supplied

[Polyamines antagonizing angiotensin II contractile effects in isolated rat aorta].

Our study showed that the administration in pre-treatment of some polyamines (especially spermine and spermidine and almost null agmatine, putrescine and cadaverine) reduced the contractile effects of angiotensin II (Ang II) in isolated rat aorta. These effects might not be associated to the interference of clathrin coated vesicles (coated pits) formation or caveolae interaction (and thus to Ang II internalization through AT1 receptors). In contrast, these effects seem to be due to the interaction with voltage-gated membrane Ca2+ channels. Therefore, the alteration of transmembrane Ca2+ fluxes does not exclude the involvement of internalization process through coated pits or caveolae, since the endocytosis mediated by these phenomena essentially needs Ca2+. In addition, the inhibitory effects are dependent on the number of positive charges of the polyamine molecules.

Algorithms↗

PubMedDate not supplied

[Interactions between angiotensin-(1-7)and angiotensin II in isolated rat portal vein].

Our preliminary data show for the first time the interaction between angiotensin-(1-7) (Ang-(1-7)) and angiotensin II (Ang II, 10 nM) in isolated rat portal vein. Very low concentrations (10 nM) of Ang-(1-7) have marked functional antagonizing effects on Ang II-induced contractions. High concentrations of Ang-(1-7) (1-10 mM) do not affect the effects of Ang II. The effects of low concentration Ang-(1-7) might be associated to the interaction with Ang-(1-7) specific receptors and the own contractile effects (approximatively 28%) at high concentrations might be assign to the interaction with angiotensin specific receptors AT1. But, the lack of effects of Ang-(1-7) high concentrations on Ang II-induced contractions hardly might be associated to the interaction with AT1 receptors. Although losartan was entirely blocking the Ang-(1-7) effects, there is in the literature a series of data showing that Ang-(1-7) specific receptors (or a subtype of Ang-(1-7) receptors) might be sensible (with possible high affinity) to losartan. Additional experiments are thus necessary to further clarify these interactions.

Algorithms↗

PubMedDate not supplied

[Cytosolic calcium dynamics and smooth muscle contraction(II): Reticular calcium fluxes].

The contractile status of smooth muscle depends upon cytosolic Ca2+, the Ca(2+)-sensitivity of actin-myosin interaction and various calcium-independent mechanisms. This second part of our overview is devoted to the complex involvement of endoplasmic reticulum in the cytosolic Ca2+ signals related to smooth muscle contractile activity, with a focus on the functional structure of reticular membrane proteins that ensure the respective Ca2+ fluxes. Ca2+ release is activated by cytosolic Ca2+, involving reticular channels called inositol triphosphate receptors and ryanodine receptors. Beside calcium and inositol triphosphate, cyclic ADP-ribose and nicotinic acid adenine dinucleotide phosphate have recently emerged as intracellular signals that activate Ca2+ release. The reticular Ca2+ pump is essential both for the control of cytosolic Ca2+ and for the preservation of reticular stores.

Calcium↗

PubMedDate not supplied

Pepstatin A is inducing contractile effects on isolated rat aorta rings.

In a series of experiments dealing with the effects of angiotensin I (AI) and angiotensinogen on isolated rat aorta we observed that pepstatin A was able to induce contractile effects by itself. The endothelin pathway was excluded by the inhibitory effects of captopril, chymostatin and amastatin. In addition, few preliminary experiments showed that the contractile effects of pepstatin A were inhibited by the pretreatment with losartan, an antagonist of AT1 angiotensin receptors. Pepstatin A-induced contractile effects on isolated rat aorta were inhibited with high potency by captopril, chymostatin and amastatin and were totally blocked by captopril + amastatin and captopril + chymostatin. Finally, we concluded that the pepstatin A-induced contractile effects on isolated rat aorta rings are dependent on an angiotensinogen vascular pool, compulsory involve an angiotensin-converting enzyme-1 (ACE-1) mediated pathway and one or more non-classical pathways for the generation of angiotensin peptides. Further experiments are necessary to elucidate the mechanisms associated to pepstatin A-induced effects.

Angiotensin I↗

PubMedDate not supplied

Are polyamines involved in the contractile effects of angiotensin II in the rat aorta? (Polyamines and angiotensin II in rat aorta).

Angiotensin II (AII) is a central factor involved in the pathophysiology of arterial hypertension and atherosclerosis. On the other hand, polyamines represent a family of organic cations with low molecular weight, playing intracellular regulatory roles essential for the cellular growth and differentiation. The cellular contents, the synthesis and the transport of polyamines are increased following the actions of AII, as well as of other cellular growth factors. Our results show that the administration of polyamines as pre-treatment modulates the contractile effects of extracellular AII (80 nM). This modulation is concentration-dependent and dual: the lower concentrations amplify and the higher concentrations reduce the effects of AII in the isolated rat aorta rings without endothelium. Moreover, DL-alpha-Difluoromethylomithine (DFMO), a specific inhibitor of ornithine decarboxylase, does not significantly modify the contractile effects of AII. Thus, these data suggest that polyamines generated through this metabolic pathway are not involved in the contractile effects of AII in rat aortic vascular smooth muscle.

Angiotensin II↗