G-protein mediated signaling pathways in myogenic responsiveness of mouse mesenteric artery

Research output: Contribution to journalConference abstract in journal

Standard

G-protein mediated signaling pathways in myogenic responsiveness of mouse mesenteric artery. / Jensen, Lars Jørn; Joseph, Philomeena Daphne; Haanes, Kristian Agmund; Hansen, Susanne Syberg; Jørgensen, Niklas Rye; Hansen, Jakob Lerche; Salomonsson, Max.

In: Microcirculation, Vol. 22, No. 7, P119, 2015, p. 631.

Research output: Contribution to journalConference abstract in journal

Harvard

Jensen, LJ, Joseph, PD, Haanes, KA, Hansen, SS, Jørgensen, NR, Hansen, JL & Salomonsson, M 2015, 'G-protein mediated signaling pathways in myogenic responsiveness of mouse mesenteric artery', Microcirculation, vol. 22, no. 7, P119, pp. 631. https://doi.org/10.1111/micc.12246

APA

Jensen, L. J., Joseph, P. D., Haanes, K. A., Hansen, S. S., Jørgensen, N. R., Hansen, J. L., & Salomonsson, M. (2015). G-protein mediated signaling pathways in myogenic responsiveness of mouse mesenteric artery. Microcirculation, 22(7), 631. [P119]. https://doi.org/10.1111/micc.12246

Vancouver

Jensen LJ, Joseph PD, Haanes KA, Hansen SS, Jørgensen NR, Hansen JL et al. G-protein mediated signaling pathways in myogenic responsiveness of mouse mesenteric artery. Microcirculation. 2015;22(7):631. P119. https://doi.org/10.1111/micc.12246

Author

Jensen, Lars Jørn ; Joseph, Philomeena Daphne ; Haanes, Kristian Agmund ; Hansen, Susanne Syberg ; Jørgensen, Niklas Rye ; Hansen, Jakob Lerche ; Salomonsson, Max. / G-protein mediated signaling pathways in myogenic responsiveness of mouse mesenteric artery. In: Microcirculation. 2015 ; Vol. 22, No. 7. pp. 631.

Bibtex

@article{356502f1667142c9a03ea488a3c99637,
title = "G-protein mediated signaling pathways in myogenic responsiveness of mouse mesenteric artery",
abstract = "Myogenic responsiveness (MR) is the ability of a small artery to constrict to an increase in intraluminal pressure and dilate to a decrease in pressure. The mechanisms linking an increase in pressure to VSMC contraction are suggested to involve mechanical activation of AT1-receptors. Our aim was to explore the role of alternative G protein-coupled receptor (GPCR) pathways. MR of pressurized mouse mesenteric arteries (MA; <200 µm) was measured as the slope of the active diameter curve. The PLC inhibitors U73122 (0.5 µM), ET-18-OCH3 (10 µM), and the PKC inhibitor BIM-X (1 µM) impaired MR. Inhibitors of PLA2 (AACOCF3, 5 µM), DAG lipase (RHC80267, 20 µM), PI3-kinase (wortmannin, 0.03 µM), CYP4A (HET0016, 10 µM), and TRPC channels (SKF96365, 10 µM) had no effects. Gq/11 and G12 mRNA and protein were expressed in MA. The Gα/q inhibitor YM-254890 (0.1 µM) and the AT1-R blocker valsartan (0.3 µM) inhibited MR. The GPCR antagonists prazosin (1 µM), losartan (0.1 µM), BQ-123 (1 µM), and SQ29548 (1 µM) had no effects. The P2Y-R antagonists suramin (100 µM) and PPADS (10 µM) inhibited MR, but the ATP diphosphatase apyrase (20 U/mL) did not. MR was similar in P2Y2-/- vs. age-matched WT mice. Preliminary data suggest a reduction of MR in P2Y6-/- mice vs. WT, and that the Rho-kinase (ROCK) inhibitor Y27632 (3 µM) inhibits MR. Thus, Gq/11 and possibly G12 pathways mediate pressure activation in mouse MA through PLC, PKC, and ROCK. MR may be initiated by mechanical activation of P2Y6-R and AT1-R in VSMCs.",
keywords = "Faculty of Health and Medical Sciences, Arterioles, myogenic tone, G-protein-coupled receptor, Purinergic receptors",
author = "Jensen, {Lars J{\o}rn} and Joseph, {Philomeena Daphne} and Haanes, {Kristian Agmund} and Hansen, {Susanne Syberg} and J{\o}rgensen, {Niklas Rye} and Hansen, {Jakob Lerche} and Max Salomonsson",
year = "2015",
doi = "10.1111/micc.12246",
language = "English",
volume = "22",
pages = "631",
journal = "Microcirculation",
issn = "1073-9688",
publisher = "JohnWiley & Sons Ltd",
number = "7",
note = "10th World Congress for Microcirculation ; Conference date: 25-09-2015 Through 27-09-2015",

}

RIS

TY - ABST

T1 - G-protein mediated signaling pathways in myogenic responsiveness of mouse mesenteric artery

AU - Jensen, Lars Jørn

AU - Joseph, Philomeena Daphne

AU - Haanes, Kristian Agmund

AU - Hansen, Susanne Syberg

AU - Jørgensen, Niklas Rye

AU - Hansen, Jakob Lerche

AU - Salomonsson, Max

PY - 2015

Y1 - 2015

N2 - Myogenic responsiveness (MR) is the ability of a small artery to constrict to an increase in intraluminal pressure and dilate to a decrease in pressure. The mechanisms linking an increase in pressure to VSMC contraction are suggested to involve mechanical activation of AT1-receptors. Our aim was to explore the role of alternative G protein-coupled receptor (GPCR) pathways. MR of pressurized mouse mesenteric arteries (MA; <200 µm) was measured as the slope of the active diameter curve. The PLC inhibitors U73122 (0.5 µM), ET-18-OCH3 (10 µM), and the PKC inhibitor BIM-X (1 µM) impaired MR. Inhibitors of PLA2 (AACOCF3, 5 µM), DAG lipase (RHC80267, 20 µM), PI3-kinase (wortmannin, 0.03 µM), CYP4A (HET0016, 10 µM), and TRPC channels (SKF96365, 10 µM) had no effects. Gq/11 and G12 mRNA and protein were expressed in MA. The Gα/q inhibitor YM-254890 (0.1 µM) and the AT1-R blocker valsartan (0.3 µM) inhibited MR. The GPCR antagonists prazosin (1 µM), losartan (0.1 µM), BQ-123 (1 µM), and SQ29548 (1 µM) had no effects. The P2Y-R antagonists suramin (100 µM) and PPADS (10 µM) inhibited MR, but the ATP diphosphatase apyrase (20 U/mL) did not. MR was similar in P2Y2-/- vs. age-matched WT mice. Preliminary data suggest a reduction of MR in P2Y6-/- mice vs. WT, and that the Rho-kinase (ROCK) inhibitor Y27632 (3 µM) inhibits MR. Thus, Gq/11 and possibly G12 pathways mediate pressure activation in mouse MA through PLC, PKC, and ROCK. MR may be initiated by mechanical activation of P2Y6-R and AT1-R in VSMCs.

AB - Myogenic responsiveness (MR) is the ability of a small artery to constrict to an increase in intraluminal pressure and dilate to a decrease in pressure. The mechanisms linking an increase in pressure to VSMC contraction are suggested to involve mechanical activation of AT1-receptors. Our aim was to explore the role of alternative G protein-coupled receptor (GPCR) pathways. MR of pressurized mouse mesenteric arteries (MA; <200 µm) was measured as the slope of the active diameter curve. The PLC inhibitors U73122 (0.5 µM), ET-18-OCH3 (10 µM), and the PKC inhibitor BIM-X (1 µM) impaired MR. Inhibitors of PLA2 (AACOCF3, 5 µM), DAG lipase (RHC80267, 20 µM), PI3-kinase (wortmannin, 0.03 µM), CYP4A (HET0016, 10 µM), and TRPC channels (SKF96365, 10 µM) had no effects. Gq/11 and G12 mRNA and protein were expressed in MA. The Gα/q inhibitor YM-254890 (0.1 µM) and the AT1-R blocker valsartan (0.3 µM) inhibited MR. The GPCR antagonists prazosin (1 µM), losartan (0.1 µM), BQ-123 (1 µM), and SQ29548 (1 µM) had no effects. The P2Y-R antagonists suramin (100 µM) and PPADS (10 µM) inhibited MR, but the ATP diphosphatase apyrase (20 U/mL) did not. MR was similar in P2Y2-/- vs. age-matched WT mice. Preliminary data suggest a reduction of MR in P2Y6-/- mice vs. WT, and that the Rho-kinase (ROCK) inhibitor Y27632 (3 µM) inhibits MR. Thus, Gq/11 and possibly G12 pathways mediate pressure activation in mouse MA through PLC, PKC, and ROCK. MR may be initiated by mechanical activation of P2Y6-R and AT1-R in VSMCs.

KW - Faculty of Health and Medical Sciences

KW - Arterioles

KW - myogenic tone

KW - G-protein-coupled receptor

KW - Purinergic receptors

U2 - 10.1111/micc.12246

DO - 10.1111/micc.12246

M3 - Conference abstract in journal

VL - 22

SP - 631

JO - Microcirculation

JF - Microcirculation

SN - 1073-9688

IS - 7

M1 - P119

T2 - 10th World Congress for Microcirculation

Y2 - 25 September 2015 through 27 September 2015

ER -

ID: 163126763