Inhibition of TRPC1/TRPC3 by PKG contributes to NO-mediated vasorelaxation.
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TRP-ing up heart and vessels: canonical transient receptor potential channels and cardiovascular diseaseTRPC1 contributes to light-touch sensation and mechanical responses in low-threshold cutaneous sensory neuronsTRPC channels and their implication in neurological diseasesNitro-oleic acid inhibits firing and activates TRPV1- and TRPA1-mediated inward currents in dorsal root ganglion neurons from adult male rats.Intrinsic phototransduction persists in melanopsin-expressing ganglion cells lacking diacylglycerol-sensitive TRPC subunitsUpregulated TRPC3 and Downregulated TRPC1 Channel Expression during Hypertension is Associated with Increased Vascular Contractility in Rat.Cholecystokinin facilitates neuronal excitability in the entorhinal cortex via activation of TRPC-like channels.Transient receptor potential channels in the vasculature.Gain-of-function mutations in transient receptor potential C6 (TRPC6) activate extracellular signal-regulated kinases 1/2 (ERK1/2)The role of cGMP/cGKI signalling and Trpc channels in regulation of vascular tone.Combined TRPC3 and TRPC6 blockade by selective small-molecule or genetic deletion inhibits pathological cardiac hypertrophy.Regulation of cardiovascular TRP channel functions along the NO-cGMP-PKG axis.cGMP becomes a drug target.Roles of ion transport in control of cell motility.Imbalance and dysfunction of transient receptor potential channels contribute to the pathogenesis of hypertension.TRPC Channels: Prominent Candidates of Underlying Mechanism in Neuropsychiatric Diseases.TRPC Channels and Stroke.Attenuation of monocyte chemotaxis--a novel anti-inflammatory mechanism of action for the cardio-protective hormone B-type natriuretic peptide.Canonical Transient Receptor Potential Channels and Their Link with Cardio/Cerebro-Vascular Diseases.Smooth Muscle Ion Channels and Regulation of Vascular Tone in Resistance Arteries and Arterioles.Chemotaxis of MDCK-F cells toward fibroblast growth factor-2 depends on transient receptor potential canonical channel 1.TRPC expression in mesenchymal stem cells.Isoform-selective physical coupling of TRPC3 channels to IP3 receptors in smooth muscle cells regulates arterial contractility.Inhibition of SOC/Ca2+/NFAT pathway is involved in the anti-proliferative effect of sildenafil on pulmonary artery smooth muscle cells.Heparin responses in vascular smooth muscle cells involve cGMP-dependent protein kinase (PKG)Role of TRPC1 and TRPC3 channels in contraction and relaxation of mouse thoracic aortaTadalafil attenuates graft arteriosclerosis of aortic transplant in a rat model.Regulation of vascular tone homeostasis by NO and H2S: Implications in hypertension.Impedance flow cytometry gauges proliferative capacity by detecting TRPC1 expression.The regulation of transient receptor potential canonical 4 (TRPC4) channel by phosphodiesterase 5 inhibitor via the cyclic guanosine 3'5'-monophosphate.
P2860
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P2860
Inhibition of TRPC1/TRPC3 by PKG contributes to NO-mediated vasorelaxation.
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article científic
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article scientifique
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articolo scientifico
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artigo científico
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bilimsel makale
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scientific article published on 05 June 2009
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vedecký článok
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vetenskaplig artikel
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videnskabelig artikel
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vědecký článek
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name
Inhibition of TRPC1/TRPC3 by PKG contributes to NO-mediated vasorelaxation.
@en
Inhibition of TRPC1/TRPC3 by PKG contributes to NO-mediated vasorelaxation.
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type
label
Inhibition of TRPC1/TRPC3 by PKG contributes to NO-mediated vasorelaxation.
@en
Inhibition of TRPC1/TRPC3 by PKG contributes to NO-mediated vasorelaxation.
@nl
prefLabel
Inhibition of TRPC1/TRPC3 by PKG contributes to NO-mediated vasorelaxation.
@en
Inhibition of TRPC1/TRPC3 by PKG contributes to NO-mediated vasorelaxation.
@nl
P2093
P2860
P1476
Inhibition of TRPC1/TRPC3 by PKG contributes to NO-mediated vasorelaxation.
@en
P2093
Muzamil M Z Noorani
Randy F Crossland
Sean P Marrelli
P2860
P304
P356
10.1152/AJPHEART.01130.2008
P577
2009-06-05T00:00:00Z