Prostaglandins as determinants of vascular reactivity.
Prostaglandins are primarily local or tissue hormones that have their effects at, or near to, the site of synthesis. Some blood vessels synthesize prostaglandins intramurally, where their local release influences vascular tone and reactivity. Endogenous prostaglandins (primarily prostaglandin E2 (PGE2) participate in the regulation of vascular reactivity by opposing the vasoconstrictor and antinatriuretic actions of circulating pressor hormones; and by braking the release of norepinephrine from vasoconstrictor nerves. The proposal that one or more prostaglandins affect vascular reactivity is supported by the following observations: enhanced vascular reactivity to pressor stimuli occurs in organs with low basal rates of prostaglandin synthesis and after inhibition of prostaglandin synthetase in organs with high biosynthetic capacity; and exogenous PGE2 reversibly inhibits the vasoconstrictor activity of pressor stimuli.
D000804:Angiotensin II / Q000494:pharmacology; D000818:Animals; D001794:Blood Pressure; D004285:Dogs; D005260:Female; D006321:Heart / Q000502:physiology*; D007668:Kidney / Q000187:drug effects / Q000502:physiology; D011247:Pregnancy; D011458:Prostaglandins E / Q000502:physiology*; D011460:Prostaglandins F / Q000502:physiology; D012039:Regional Blood Flow / Q000187:drug effects; D014599:Uterus / Q000187:drug effects / Q000502:physiology
D011458:Prostaglandins E; D011460:Prostaglandins F; D000804:Angiotensin II