Wyniki wyszukiwania

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ACE inhibitor and AT1 antagonist stimulate duodenal HCO3 secretion mediated by a common pathway - involvement of PG, NO and bradykinin

100%

Aihara E., Kagawa S., Hayashi M., Takeuchi K.

Journal of Physiology and Pharmacology

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2005

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tom 56

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nr 3

Recent study demonstrated that duodenal HCO3- secretion is affected by modulation of the renin-angiotensin system. We examined the effects of enalapril (angiotensin-converting enzyme (ACE) inhibitor) or losartan (angiotensin AT1 receptor antagonist) on duodenal HCO3- secretion in rats and investigated the mechanisms involved in the renin-angiotensin system-related HCO3- response. A proximal duodenal loop was perfused with saline, and HCO3- secretion was measured at pH 7.0 using a pH-stat method and by adding 2 mM HCl. Enalapril increased the HCO3- secretion in a dose-dependent manner, with a decrease in arterial blood pressure (MBP), and these effects were significantly attenuated by pretreatment with indomethacin, L-NAME and FR172357 (a selective bradykinin B2 receptor antagonist). Although losartan alone did not affect the HCO3- secretion, despite reducing MBP, the agent dose-dependently increased the HCO3- secretion in the presence of angiotensin II, and this response was totally antagonized by prior administration of FR172357, indomethacin and L-NAME. Bradykinin also dose-dependently increased the HCO3- secretion with no change in MBP, though transient, and again the effects were blocked by indomethacin, L-NAME and FR172357. Both prostaglandin (PG) E2 and the nitric oxide (NO) donor NOR-3 also increased the HCO3- secretion, the latter effect being inhibited by indomethacin. These results suggest that both an ACE inhibitor and AT1 antagonist (in the presence of angiotensin II) increase duodenal HCO3- secretion via a common pathway, involving bradykinin, NO and PGs. It is also assumed that bradykinin releases NO locally, which in turns stimulates HCO3- secretion mediated by PGs.

2

Measurement of angiotensin metabolites in organ bath and cell culture experiments by liquid chromatography - electrospray ionization - mass epectrometry (LC-ESI-MS)

100%

Bujak-Gizycka B., Madej J., Wolkow P. P., Olszanecki R., Drabik L., Rutowski J., Korbut R.

Journal of Physiology and Pharmacology

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2007

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tom 58

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nr 3

The metabolism of renin-angiotensin system (RAS) is more complicated than previously expected and understanding the biological phenomena regulated by variety of angiotensin metabolites requires their precise and possibly comprehensive quantitation. Physiological concentrations of angiotensins (Ang) in biological fluids are low, therefore their accurate measurements require very sensitive and specific analytical methods. In this study we developed an accurate and reproducible method of quantitation of angiotensin metabolites through coupling of liquid chromatography and electrospray ionization - mass spectrometry (LC-ESI-MS). With this method main angiotensin metabolites (Ang I, II, III, IV, 1-9, 1-7, 1-5) can be reliably measured in organ bath of rat tissues (aorta, renal artery, periaortal adipose tissue) and in medium of cultured endothelial cells (EA.hy926), exposed to Ang I for 15 minutes, in the absence or in the presence of angiotensin converting enzyme inhibitor, perindoprilat. Presented LC-ESI-MS method proved to be a quick and reliable solution to comprehensive analysis of angiotensin metabolism in biological samples.

3

Angiotensin-[1-9], the product of angiotensin I conversion in platelets, enhances arterial thrombosis in rats

84%

Kramkowski K., Mogielnicki A., Leszczynska A., Buczko W.

Journal of Physiology and Pharmacology

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2010

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tom 61

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nr 3

317-324

Angiotensin (Ang) (1-9) is the renin-angiotensin-system peptide found in the plasma of healthy volunteers and after angiotensin-converting-enzyme inhibitors therapy. In vitro experiments proved that Ang-(1-9) may be produced from Ang I. In our study, we tried to expand the poor data about the in vivo properties of Ang-(1-9). We revealed that Ang-(1-9) enhanced electrically stimulated arterial thrombosis in the carotid artery of Wistar rats. Losartan, a selective blocker of AT1 receptor for Ang II, abolished the prothrombotic activity of Ang-(1-9). This peptide increased plasma level of fibrinogen, augments fibrin generation, and similarly to Ang II, potentiated collagen induced platelet aggregation. Using HPLC, we found that after incubation of Ang-(1-9) with platelet homogenates or after intravenous administration this peptide is converted to Ang II. We concluded that Ang-(1-9) exerts an Ang II-like prothrombotic effect due to the conversion to Ang II in the circulatory system of rats and that platelets are involved in this process.

4

Kaempferol, but not resveratrol inhibits angiotensin converting enzyme

84%

Olszanecki R., Bujak-Gizycka B., Madej J., Suski M., Wolkow P. P., Jawien J., Korbut R.

Journal of Physiology and Pharmacology

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2008

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tom 59

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nr 2

Inhibition of angiotensin converting enzyme (ACE) has proved to be beneficial in the treatment of various cardiovascular disorders. The aim of this study was to evaluate ACE inhibitory potential of two polyphenolic compounds with different structures: resveratrol (present in high quantities in French wine) and kaempferol (abundant in greens), using method of liquid chromatography coupled with electrospray ionization mass spectrometry (LC-ESI-MS) for ex vivo measurement of angiotensin I to angiotensin II conversion by ACE in aortic tissue of Wistar-Kyoto rats. In this setting, kaempferol (10-30-100 µM), but not resveratrol (10-30-100 µM) appeared to inhibit dose-dependently conversion of Ang I to Ang II. Although the mechanism of ACE inhibition by kaempferol remains to be elucidated, this observation may help in search or designing of new classes of ACE inhibitors.

5

Pathways of glomerular toxicity of cyclosporine-A: an "in vitro" study

84%

Castello L., Sainaghi P. P., Bergamasco L., Letizia C., Bartoli E.

Journal of Physiology and Pharmacology

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2005

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tom 56

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nr 4

Background/Aims. Knowledge of renal toxicity of cyclosporine-A (CyA) is clouded by multiple effects on different glomerular and tubular cells and on kidney and systemic hemodynamics. To focus on glomerular action of CyA we used glomeruli isolated in vitro, with the aim of dissecting the effects on recruitment of glomerular vasoconstricting systems, like endothelin-1 (ET) and angiotensins (AI and AII). Methods. We studied the pathways of CyA damage on pig glomeruli isolated in vitro with the technique of sieving through mesh filters of different sizes, and incubated in an appropriate culture medium. The supernatant was sampled at different time intervals to measure ET, AI and AII concentrations upon addition of ET 10-12 or CyA 4·10-7 M, with or without either selective endothelin receptor A (ETA) or B (ETB), or unselective ETA-ETB receptor inhibitors. Results. CyA increased ET concentration (from 9.7±0.3 to 11.4±0.4 pg·ml-1, p<0.002), and the added ET released AI in the medium (from 26.6±4.7 to 39.1±4.6 pg·ml-1, p<0.05) when ETB receptors were blocked. In contrast, CyA stimulated angiotensins release independent of ET receptors blockade, hence, irrespective of ET concentration in the medium, from 26.6±4.7 to 38.0±2.1 pg·ml-1 for AI, p<0.05, and from 12.3±1.0 to 14.8±0.9 pg·ml-1 for AII, p<0.05. Conclusion. CyA releases ET and angiotensins independently by a direct action. Glomerular CyA toxicity might be mediated by recruitment of vasoconstricting peptides and modulated by relative ETA and ETB receptor occupancy.

6

Effect of converting enzyme inhibitor on copper and iron concentrations of blood plasma in calves during the neonatal period

67%

Skrzypczak W., Dratwa-Chalupnik A., Ozgo M., Michalek K., Lepczynski A., Hejza K., Siwa J.

Folia Biologica

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2010

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tom 58

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nr 1-2

119-124

Ograniczanie wyników

ACE inhibitor and AT1 antagonist stimulate duodenal HCO3 secretion mediated by a common pathway - involvement of PG, NO and bradykinin

Measurement of angiotensin metabolites in organ bath and cell culture experiments by liquid chromatography - electrospray ionization - mass epectrometry (LC-ESI-MS)

Angiotensin-[1-9], the product of angiotensin I conversion in platelets, enhances arterial thrombosis in rats

Kaempferol, but not resveratrol inhibits angiotensin converting enzyme

Pathways of glomerular toxicity of cyclosporine-A: an "in vitro" study

Effect of converting enzyme inhibitor on copper and iron concentrations of blood plasma in calves during the neonatal period