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001-es BibID:BIBFORM061585
Első szerző:Csongrádi Éva (szakorvos)
Cím:Renal Inhibition of Heme Oxygenase-1 Increases Blood Pressure in Angiotensin II-Dependent Hypertension / Csongradi, E., Storm, M. V., Stec, D. E.
Dátum:2012
Megjegyzések:The goal of this study was to test the hypothesis that renal medullary heme oxygenase (HO) acts as a buffer against Ang-IIdependent hypertension. To test this hypothesis, renal medullary HO activity was blocked using QC-13, an imidazole-dioxolaneHO-1 inhibitor, or SnMP, a classical porphyrin based HO inhibitor. HO inhibitors were infused via IRMI catheters throughout thestudy starting 3 days prior to implantation of an osmotic minipump which delivered Ang II or saline vehicle. MAP was increasedby Ang II infusion and further increased by IRMI infusion of QC-13 or SnMP.MAP averaged 113?3, 120?7, 141?2, 153?2, and154?3mmHg in vehicle, vehicle + IRMI QC-13, Ang II, Ang II + IRMI QC-13, and Ang II + IRMI SnMP treated mice, respectively(n = 6). Inhibition of renal medullaryHO activity with QC-13 in Ang II infused mice was also associated with a significant increasein superoxide production as well as significant decreases in antioxidant enzymes catalase and MnSOD. These results demonstratethat renal inhibition of HO exacerbates Ang II dependent hypertension through a mechanism which is associated with increasesin superoxide production and decreases in antioxidant enzymes.
Tárgyszavak:Orvostudományok Egészségtudományok idegen nyelvű folyóiratközlemény külföldi lapban
Heme Oxygenase-1
Angiotensin II
Hypertension
Megjelenés:International Journal of Hypertension 2012 (2012), p. Article ID 497213. -
További szerzők:Storm, Megan V. Stec, David E.
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001-es BibID:BIBFORM061587
Első szerző:Stec, David E.
Cím:Expression of Heme Oxygenase-1 in Thick Ascending Loop of Henle Attenuates Angiotensin II-Dependent Hypertension / David E. Stec, Heather A. Drummond, Monette U. Gousette, Megan V. Storm, Nader G. Abraham, Eva Csongradi
Dátum:2012
Megjegyzések:Kidney-specific induction of heme oxygenase-1 (HO-1) attenuates the development of angiotensin II (AngII) -dependent hypertension, but the relative contribution of vascular versus tubular induction of HO-1 isunknown. To determine the specific contribution of thick ascending loop of Henle (TALH) -derived HO-1,we generated a transgenic mouse in which the uromodulin promoter controlled expression of human HO-1.Quantitative RT-PCR and confocal microscopy confirmed successful localization of the HO-1 transgeneto TALH tubule segments. Medullary HO activity, but not cortical HO activity, was significantly higher intransgenic mice than control mice. Enhanced TALH HO-1 attenuated the hypertension induced by Ang IIdelivered by an osmotic minipump for 10 days (13963 versus 15362 mmHg in the transgenic and controlmice, respectively; P,0.05). The lower blood pressure in transgenic mice associated with a 60% decreasein medullary NKCC2 transporter expression determined by Western blot. Transgenic mice also exhibited a36% decrease in ouabain-sensitive sodium reabsorption and a significantly attenuated response to furosemidein isolated TALH segments,. In summary, these results show that increased levels of HO-1 in theTALH can lower blood pressure by a mechanism that may include alterations in NKCC2-dependent sodiumreabsorption.
Tárgyszavak:Orvostudományok Egészségtudományok idegen nyelvű folyóiratközlemény külföldi lapban
Heme Oxygenase-1, Angiotensin II, Hypertension
Megjelenés:Journal of the American Society of Nephrology. - 23 : 5 (2012), p. 834-841. -
További szerzők:Drummond, Heather A. (tudományos segédmunkatárs) Gousette, Monette U. (orvos) Storm, Megan V. Abraham, Nader G. (tudományos segédmunkatárs) Csongrádi Éva (1969-) (szakorvos)
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