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Biomedical subjects

M Costuleanu

Publications and source records attributed to M Costuleanu.

29 records · Page 2Linked to original sources
PubMedDate not supplied

[Xanthine derivative compounds potential activity in inflammatory process].

We studied the potentially anti-inflammatory action of some new xanthine compounds, theophylline derivatives with 7-[2-hydroxy-3-(4-acetamido)-phenoxy-propyl]-8-R-1,3-dimethyl-xanthine and 8-R-1,3-bis-(1,3-dimethyl-xanthin-7yl)-2-hydroxy-propane structure substituted in 7 and 8 position. Almost all studied compounds reduced the inflammatory edema, the effect being comparable or highest theophylline. The antiinflammatory effect of theophylline intensified with the introduction in 7 position the theophylinyl radical and in 8 position the bromo, nitro, pirolidinyl, piperidinyl, morfolinyl, imidazolyl, 3,5-dimethyl-pirazolyl, 3-methyl-5-oxo-pirazolyl radicals.

Animals↗
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[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.

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[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.

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[Alternative pathways for the activation of the renin-angiotensin system].

The knowledge of the structure and function of the components of the renin-angiotensin system (RAS) is rapidly increasing. The classic pathway of angiotensin (Ang) II generation includes a reaction catalyzed by angiotensin-converting enzyme (ACE). We actually discuss the alternative pathways for the generation of Ang-II and other angiotensin peptides (Ang III, Ang IV, Ang (1-9), Ang (1-7), des-Asp-Ang I) and the responsible enzymes (tonins, cathepsins, chymases, aminopeptidases, dipeptidyl aminopeptidases, neutral endopeptidases, carboxypeptidases, ACE2 etc.). The development of novel enzyme inhibitors (e.g., nafamostat, sampatrilat) for more efficacious suppression of RAS activity is also considered.

Angiotensin II↗
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↗
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Interactions between extracellular and intracellular administered angiotensin II in isolated rat portal vein rings.

It is already demonstrated that intracellular angiotensin II (Ang II) stimulates smooth muscle contraction and cell growth. We studied the contractile effects of Ang II intracellular delivered by the means of liposomes (LAngII) and also the interactions between intracellular and extracellular administered Ang II on the rat portal vein rings without endothelium. The results were expressed as the percentages of the control contraction (K+ 40 mM; mean +/- S.E.M). LAngII induced contractions were of 120.46 +/- 8.06%. On the other hand, 0.1 microM Ang II produced contractions of 121.43 +/- 6.83%. Both Ang II and losartan, administered either extracellular in the organ bath or intracellular by the means of liposomes, inhibited the contractions induced by intracellular Ang II. The inhibitory effects of losartan on LAngII-induced contractions were dose-dependent. Thus, 10 microM losartan strongly blocked (10.01 +/- 1.41%) and 1 microM losartan partially blocked (39.73 +/- 5.35%) the LAngII-induced effects. LLOS significantly inhibited the LAngII contractile effects (38.51 +/- 8.92%). Our results revealed that LAngII partially inhibited the contractions induced by extracellular administered Ang II (42.42 +/- 3.29%). On the other hand, 0.1 microM Ang II also inhibited the contractile effects induced by LAngII (67.42 +/- 0.76%), although a little bit less. So, contractions induced by Ang II administered intracellular are mainly mediated by intracellular Ang II receptors sensitive to losartan. At the same time, the participation of cell membrane angiotensin receptors to intracellular Ang II effects cannot be excluded.

Algorithms↗
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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↗
PubMedDate not supplied

Researches on the influence of some pharmacological interferences of the metabolism of icosanoids on the glycemia in rats.

We studied the influence of cloprostenol (CIPG) 200 micrograms/Kg i.p. (a synthetic analogue of PGF2-alpha) and of imidazol 70 mg/Kg i.p. (a selective inhibitor of thromboxane synthetase) on fasting glycemia and on hypoglycemia induced by Actrapid insulin 0.5 UI/Kg i.p. to rats (male adults). The determinations of glycemia were made 60 minutes and 3 hours after the administration of the substances. The tests were made in groups of 20 animals which were not fed 14 hours before the experiment, but were not deprived of water. The results were interpreted statistically by means of the "t" test. The data obtained show that CIPG 200 micrograms/Kg i.p. is a significant hyperglycemic icosanoid (statistically p less than 0.01) both in the case of fasting glycemia and in the case of insulin hypoglycemia. The hyperglycemic effect was stronger at 60 min. Imidazol does not modify significantly either glycemia or insulin hypoglycemia, which pleads for a more reduced implication of thromboxanes in the regulation of glycemia in comparison to the prostaglandins.

Animals↗
PubMedDate not supplied

The influence of an PGF2x analogue and of some peptidoleukotrienes and platelet activating factor antagonists in experimentally induced gastric ulcer in rats.

We tested the influence of 30 mg/kg/per os BN 52021, 300 micrograms/kg Cloprostenol (CIPG) and of 5 mg/kg per os LY 171883B in stress restrain and indomethacin induced ulcers in rats. The data obtained show that CIPG and LY 171883 have a significant gastroprotective action in both ulcer models. BN 52021 has a significant protective activity in stress ulcer and less in indomethacin-induced ulcers.

Acetophenones↗