Cardiovascular prostaglandins: some comments on their involvement in circulatory physiology and pathophysiology.
There is little, if any, good evidence in the literature to indicate a role for cardiovascular PG in congestive heart failure, either in its pathogenesis or as a consequence of and defense against its manifestations. Usually congestive heart failure is considered to develop as a vicious cycle in which impaired cardiac output, increased peripheral resistance, decreased renal blood flow, increased renin release and further increased peripheral resistance and decreased cardiac output are important constituents. Increased sympathetic activity may promote cardiovascular PG formation through the sympathetic neurotransmitter noradrenaline; such an action has, however, not been documented hitherto. Furthermore, increased plasma renin activity may promote PG formation via increased circulating levels of angiotensin; even such an action remains, however, to be demonstrated. If the heart failure leads to local tissue ischemia the hypoxia as such, or the subsequent increase in adenosine production, may also facilitate cardiovascular PG formation. All these mechanisms, if operative, would counteract the increased peripheral resistance, by promoting the formation of vasodilator PG. On the other hand PGI2 stimulates renal formation of renin, which would act to elevate the peripheral resistance. These contradictory effects of endogenously formed PG focus on the need for more careful studies on their involvement in the hemodynamic consequences of congestive heart failure: until more data are available it is impossible to know whether an activated synthesis of PG should be regarded as advantageous and worth therapeutical support, or negative and subject to inhibition.(ABSTRACT TRUNCATED AT 250 WORDS)
D015121:6-Ketoprostaglandin F1 alpha / Q000097:blood; D015237:Dinoprost; D015232:Dinoprostone; D011464:Epoprostenol / Q000378:metabolism; D006333:Heart Failure / Q000503:physiopathology*; D006801:Humans; D007213:Indomethacin / Q000494:pharmacology; D007668:Kidney / Q000502:physiology; D011448:Prostaglandin Antagonists / Q000494:pharmacology; D011453:Prostaglandins / Q000502:physiology*; D011458:Prostaglandins E / Q000096:biosynthesis; D011460:Prostaglandins F / Q000096:biosynthesis; D013928:Thromboxane A2 / Q000096:biosynthesis
D011448:Prostaglandin Antagonists; D011453:Prostaglandins; D011458:Prostaglandins E; D011460:Prostaglandins F; D013928:Thromboxane A2; D015121:6-Ketoprostaglandin F1 alpha; D015237:Dinoprost; D011464:Epoprostenol; D015232:Dinoprostone; D007213:Indomethacin