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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
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001-es BibID:BIBFORM029131
Első szerző:Beleznai Tímea (orvos)
Cím:Smooth Muscle Ca2+-Activated and Voltage-Gated K+ Channels Modulate Conducted Dilation in Rat Isolated Small Mesenteric Arteries / Beleznai T. Z., Yarova P. L., Yuill K. H., Dora K. A.
Dátum:2011
ISSN:1073-9688
Megjegyzések:To assess the influence of blocking smooth muscle large conductance Ca(2+) -activated K+ channels and voltage-gated K+ channels on the conducted dilation to ACh and isoproterenol. MATERIALS AND METHODS: Rat mesenteric arteries were isolated with a bifurcation, triple-cannulated, pressurized and imaged using confocal microscopy. Phenylephrine was added to the superfusate to generate tone, and agonists perfused into a sidebranch to evoke local dilation and subsequent conducted dilation into the feed artery. RESULTS: Both ACh- and isoproterenol-stimulated local and conducted dilation with similar magnitudes of decay with distance along the feed artery (2000 m: 15% maximum dilation). The gap junction uncoupler carbenoxolone prevented both conducted dilation and intercellular spread of dye through gap junctions. IbTx, TEA or 4-AP, blockers of large conductance Ca(2+) -activated K+ channels and voltage-gated K+ channels, did not affect conducted dilation to either agonist. A combination of either IbTx or TEA with 4-AP markedly improved the extent of conducted dilation to both agonists (2000 m: >50% maximum dilation). The enhanced conducted dilation was reflected in the hyperpolarization to ACh (2000 m: Control, 4±1 mV, n = 3; TEA with 4-AP, 14±3mV, n=4), and was dependent on the endothelium. CONCLUSIONS: These data show that activated BK(Ca) and K(V) -channels serve to reduce the effectiveness of conducted dilation.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Microcirculation. - 18 : 6 (2011), p. 487-500. -
További szerzők:Yarova, Polina L. Yuill, Kathryn H. Dora, Kim A.
Pályázati támogatás:British Heart Foundation
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Intézményi repozitóriumban (DEA) tárolt változat
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