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001-es BibID:	BIBFORM029130
Első szerző:	Beleznai Tímea (orvos)
Cím:	Enhanced K+-channel-mediated endothelium-dependent local and conducted dilation of small mesenteric arteries from ApoE-/- mice / Beleznai T., Takano H., Hamill C., Yarova P., Douglas G., Channon K., Dora K.
Dátum:	2011
ISSN:	0008-6363
Megjegyzések:	Agonists that evoke smooth muscle cell hyperpolarization have the potential to stimulate both local and conducted dilation. We investigated whether the endothelium-dependent vasodilators acetylcholine (ACh) and SLIGRL stimulated conducted dilation and whether this was altered by deficiency in apolipoprotein E (ApoE-/-). Methods and results Isolated mesenteric arteries were cannulated, pressurized, and precontracted with phenylephrine. Agonists were either added to the bath to study local dilation or were restricted to one end of arteries to study conducted dilation. An enhanced sensitivity to both ACh and SLIGRL was observed in mesenteric arteries from ApoE-/- mice compared with wild-type controls. Inhibition of nitric oxide (NO) synthase blocked ACh responses, but had no effect on maximum dilation to SLIGRL. SLIGRL increased endothelial cell Ca2+, hyperpolarized smooth muscle cells, and fully dilated arteries. The NO-independent dilation to SLIGRL was blocked with high [KCl] or Ca2+-activated K+-channel blockers. The hyperpolarization and dilation to SLIGRL passed through the artery to at least 2.5 mm upstream. The conducted dilation was not affected by a deficit in ApoE and could also be stimulated by ACh, suggesting NO itself could stimulate conducted dilation. Conclusion In small mesenteric arteries of ApoE-/- mice, NO-independent dilation is enhanced. Since both NO-dependent and -independent pathways can stimulate local and conducted dilation, the potential for reducing vascular resistance is improved in these vessels.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:	Cardiovascular Research. - 92 : 2 (2011), p. 199-208. -
További szerzők:	Takano, Hiromichi Hamill, Claire Yarova, Polina L. Douglas, Gillian Channon, Keith Dora, Kim A.
Pályázati támogatás:	British Heart Foundation Egyéb
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM018438
Első szerző:	Fehér Attila (orvos)
Cím:	Caveolin-1 limits the contribution of BK(Ca) channel to EDHF-mediated arteriolar dilation: implications in diet-induced obesity / Feher, A., Rutkai, I., Beleznai, T., Ungvari, Z., Csiszar, A., Edes, I., Bagi, Z.
Dátum:	2010
ISSN:	0008-6363
Megjegyzések:	Caveolin-1 (Cav-1) interacts with large conductance Ca(2+)-activated potassium channels (BKCa) and likely exerts a negative regulatory effect on the channel activity. We investigated the role of Cav-1 in modulating BK(Ca) channel-mediated, endothelium-derived hyperpolarizing factor (EDHF)-dependent arteriolar dilation in normal condition and in an experimental model of obesity. METHODS AND RESULTS: In isolated, pressurized (80 mmHg) gracilis muscle arterioles (approximately 100 microm) of Cav-1 knockout mice, acetylcholine (ACh)-induced, EDHF-mediated dilations were enhanced and were significantly reduced by the BK(Ca) channel inhibitor, iberiotoxin (IBTX), whereas IBTX had no effect on EDHF-mediated dilations in the wild-type mice. Dilations to the selective BK(Ca) channel opener, NS-1619 were augmented in the Cav-1 knockout mice. In high-fat diet-treated, obese rats ACh-induced coronary arteriolar dilations were preserved, whereas IBTX-sensitive, ACh-induced and also NS-1619-evoked vasodilations were augmented when compared with lean animals. In coronary arterioles of obese rats a reduced protein expression of Cav-1 was detected by western immunoblotting and immunohistochemistry. Moreover, in coronary arterioles of lean rats, disruption of caveolae with methyl-beta-cyclodextrin augmented IBTX-sensitive, ACh-induced, and also NS-1619-evoked dilations. CONCLUSION: Thus, under normal conditions, Cav-1 limits the contribution of the BK(Ca) channel to EDHF-mediated arteriolar dilation. In obesity, a reduced expression of Cav-1 leads to greater contribution of the BK(Ca) channel to EDHF-mediated response, which seems essential for maintained coronary dilation.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban Coronary Microcirculation EDHF MaxiK channel Caveolae
Megjelenés:	Cardiovascular Research. - 87 : 4 (2010), p. 732-739. -
További szerzők:	Rutkai Ibolya (1985-) (molekuláris biológus) Beleznai Tímea (1981-) (orvos) Ungvári Zoltán Csiszár Anna Édes István (1952-) (kardiológus) Bagi Zsolt (1974-) (orvos)
Pályázati támogatás:	0735540T Egyéb
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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