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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 Egyéb
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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