Lysophosphatidic acid acts on LPA₁ receptor to increase H₂ O₂ during flow-induced dilation in human adipose arterioles.

ABSTRACT:

Background and purpose

NO produces arteriolar flow-induced dilation (FID) in healthy subjects but is replaced by mitochondria-derived hydrogen peroxide (mtH₂ O₂ ) in patients with coronary artery disease (CAD). Lysophosphatidic acid (LPA) is elevated in patients with risk factors for CAD, but its functional effect in arterioles is unknown. We tested whether elevated LPA changes the mediator of FID from NO to mtH₂ O₂ in human visceral and subcutaneous adipose arterioles.

Experimental approach

Arterioles were cannulated on glass micropipettes and pressurized to 60 mmHg. We recorded lumen diameter after graded increases in flow in the presence of either NOS inhibition (L-NAME) or H₂ O₂ scavenging (Peg-Cat) ± LPA

SUBMITTER: Chabowski DS 

PROVIDER: S-EPMC6193883 | biostudies-literature | 2018 Nov

REPOSITORIES: biostudies-literature