| First Author | Wegener JW | Year | 2014 |
| Journal | FASEB J | Volume | 28 |
| Issue | 3 | Pages | 1044-8 |
| PubMed ID | 24253251 | Mgi Jnum | J:210378 |
| Mgi Id | MGI:5570982 | Doi | 10.1096/fj.13-237925 |
| Citation | Wegener JW, et al. (2014) Phospholipase D1 is involved in alpha1-adrenergic contraction of murine vascular smooth muscle. FASEB J 28(3):1044-8 |
| abstractText | alpha1-Adrenergic stimulation increases blood vessel tone in mammals. This process involves a number of intracellular signaling pathways that include signaling via phospholipase C, diacylglycerol (DAG), and protein kinase C. So far, it is not certain whether signaling via phospholipase D (PLD) and PLD-derived DAG is involved in this process. We asked whether PLD participates in the alpha1-adrenergic-mediated signaling in vascular smooth muscle. alpha1-Adrenergic-induced contraction was assessed by myography of isolated aortic rings and by pressure recordings using the hindlimb perfusion model in mice. The effects of the PLD inhibitor 1-butanol (IC50 0.15 vol%) and the inactive congener 2-butanol were comparatively studied. Inhibition of PLD by 1-butanol reduced specifically the alpha1-adrenergic-induced contraction and the alpha1-adrenergic-induced pressure increase by 10 and 40% of the maximum, respectively. 1-Butanol did not influence the aortic contractions induced by high extracellular potassium, by the thromboxane analog U46619, or by a phorbol ester. The effects of 1-butanol were absent in mice that lack PLD1 (Pld1(-/-) mice) or that selectively lack the CaV1.2 channel in smooth muscle (sm-CaV1.2(-/-) mice) but still present in the heterozygous control mice. alpha1-Adrenergic contraction of vascular smooth muscle involves activation of PLD1, which controls a portion of the alpha1-adrenergic-induced CaV1.2 channel activity. |
