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Tytuł pozycji:

The role of cGMP/cGKI signalling and Trpc channels in regulation of vascular tone.

Tytuł :
The role of cGMP/cGKI signalling and Trpc channels in regulation of vascular tone.
Autorzy :
Loga, Florian
Domes, Katrin
Freichel, Marc
Flockerzi, Veit
Dietrich, Alexander
Birnbaumer, Lutz
Hofmann, Franz
Wegener, Jörg W.
Pokaż więcej
Temat :
VASCULAR smooth muscle
PROTEIN kinases
CELLULAR signal transduction
TRP channels
ENDOTHELIAL cells
LABORATORY mice
IMMUNOCYTOCHEMISTRY
NITRIC oxide
PHENYLEPHRINE
Źródło :
Cardiovascular Research; Nov2013, Vol. 100 Issue 2, p280-287, 8p
Czasopismo naukowe
Aims Signalling via cGMP-dependent protein kinase I (cGKI) is the major pathway in vascular smooth muscle (SM), by which endothelial NO regulates vascular tone. Recent evidence suggests that canonical transient receptor potential (Trpc) channels are targets of cGKI in SM and mediate the relaxant effects of cGMP signalling. We tested this concept by investigating the role of cGMP/cGKI signalling on vascular tone and peripheral resistance using Trpc6−/−, Trpc3−/−, Trpc3−/−/6−/−, Trpc1−/−/3−/−/6−/−, and SM-specific cGKI−/− (sm-cGKI−/−) mice. Methods and results α-Adrenergic stimulation induced similar contractions in L-NG-nitroarginine methyl ester (l-NAME)-treated aorta and comparably increased peripheral pressure in hind limbs from all mouse lines investigated. After α-adrenergic stimulation, 8-Br-cGMP diminished similarly aortic tone and peripheral pressure in control, Trpc6−/−, Trpc3−/−, Trpc3−/−/6−/−, and Trpc1−/−/3−/−/6−/− mice but not in sm-cGKI−/− mice. In untreated aorta, α-adrenergic stimulation induced similar contractions in the aorta from control and Trpc3−/− mice but larger contractions in sm-cGKI−/−, Trpc6−/−, Trpc3−/−/6−/−, and Trpc1−/−/3−/−/6−/− mice, indicating a functional link between cGKI and Trpc6 channels. Trpc3 channels were detected by immunocytochemistry in both isolated aortic smooth muscle cells (SMCs) and aortic endothelial cells (ECs), whereas Trpc6 channels were detected only in ECs. Phenylephrine-stimulated Ca2+ levels were similar in SMCs from control (Ctr) and Trpc6−/− mice. Carbachol-stimulated Ca2+ levels were reduced in ECs from Trpc6−/− mice. Stimulated Ca2+ levels were lowered by 8-Br-cGMP in Ctr but not in Trpc6−/− ECs. Conclusions The results suggest that cGKI and Trpc1,3,6 channels are not functionally coupled in vascular SM. Deletion of Trpc6 channels impaired endothelial cGKI signalling and vasodilator tone in the aorta. [ABSTRACT FROM AUTHOR]
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