Modification of adrenergic and vasopressin receptor-linked lipid metabolism during endotoxemia.
Our studies addressing various aspects of lipid metabolism linked to the activation of alpha 1-adrenergic and vasopressin receptors suggest the following conclusions: 1) Adjustments in lipid metabolic flux seem to compensate for catabolic processes known to be triggered by endotoxin; 2) the diminished DG signal generation for vasopressin1 receptor-linked transduction mechanisms is likely to underlie some concomitant functional impairments and 3) defective acylation of AA may contribute to cellular metabolic perturbations by affecting the turnover of PI, a phospholipid involved in signal transmission, and leading to increased availability of AA for eicosanoid synthesis.
Spitzer
J A
JA
Department of Physiology, Louisiana State University Medical Center, New Orleans 70112.
Rodriguez de Turco
E B
EB
D000818:Animals; D001095:Arachidonic Acids / Q000378:metabolism; D002462:Cell Membrane / Q000378:metabolism; D008099:Liver / Q000378:metabolism*; D008563:Membrane Lipids / Q000378:metabolism; D051381:Rats; D011942:Receptors, Adrenergic, alpha / Q000378:metabolism*; D011945:Receptors, Angiotensin / Q000378:metabolism*; D017483:Receptors, Vasopressin; D012016:Reference Values; D015290:Second Messenger Systems; D012772:Shock, Septic / Q000378:metabolism*; D010738:Type C Phospholipases / Q000378:metabolism; D014667:Vasopressins / Q000378:metabolism*
D001095:Arachidonic Acids; D008563:Membrane Lipids; D011942:Receptors, Adrenergic, alpha; D011945:Receptors, Angiotensin; D017483:Receptors, Vasopressin; D014667:Vasopressins; D010738:Type C Phospholipases