Atherosclerosis decreased prostacyclin formation in rabbit lungs and kidneys

Lipid composition of rabbit aortic wall following removal of endothelium by balloon catheter.

“…In summarizing their observations in many specimens of atherosclerotic human and animal tissues, Sinzinger et al 24 reported a diminished formation of prostacyclin. Similar data were published by Dembinska-Kiec et al 25 indicating that atherosclerosis decreases prostacyclin formation in rabbit lungs and kidneys, thereby implying an alteration in the metabolism of arachidonic acid. Our results did not show any tendency to regression, a characteristic feature of the lesions developed by repeated or continued injury, 26 reflecting different responses to various types of injury.…”

Prostacyclin and Hypertension

“…Among the prostaglandins with a vasodepressor effect, prostacyclin, as the main vascular prostaglandin, probably plays the leading part in blood pressure regulation. This finding is possibly explained by the marked atherosclerotic vascular changes in these animals, for with increasing atherosclerosis of the vessels their rate of prostacyclin synthesis continuously declines [47,95,139]. Locally, prostacyclin synthesis appears to be increased in spontaneously hypertensive rats.…”

“…The total radioactivity obtained from the TLC plates was defined as 100% (x ± SEM; * P < 0.02; ** P < 0.005) [47] * p < 0.05; *** P < 0.001; number of patients in column) [125] and in vessels with an endothelial-free neointima from smooth muscle [58,59]. A dietetically induced hypercholesteremia ( Fig.…”

“…Prostacyclin may be of very considerable importance in this interrelation since it can no longer be synthesized in normal concentrations by vessels affected by atherosclerosis [47,95,138,139]. Prostacyclin may be of very considerable importance in this interrelation since it can no longer be synthesized in normal concentrations by vessels affected by atherosclerosis [47,95,138,139].…”

Pathophysiology of the hepoxilins

“…These channels open as a response to the stimulated depletion of Ca 2+ through interaction with IP3 and its receptor IP3R. IP3 and DAG are generated from PIP2 upon activation of PLC [88,89]. Indeed it has been shown that hepoxilin A 3 activated the release of DAG from human neutrophils [90].…”