Vascular and renal prostaglandins as counter-regulatory systems in heart failure.
Vasoconstrictors and vasodilators are both activated in patients with severe heart failure. Vasodilatory prostaglandins are increased in parallel with the degree of activation of neurohumoral vasoconstrictor systems, and may serve to offset the circulatory effects of systemic and regional vasoconstriction. Enhanced vasoconstrictive and vasodilatory activities appear to be especially important in patients with hyponatraemia. These patients may be particularly susceptible to clinical deterioration when given drugs that inhibit prostaglandin synthesis (e.g. indomethacin) and may be more likely to improve when treated with agents that enhance the production of endogenous prostaglandin (e.g. angiotensin converting enzyme inhibitor). Exogenous PGE2 reduces afterload and may be a useful therapeutic agent. Research on vascular and renal prostaglandins should further our knowledge of the pathophysiology and therapy of congestive heart failure.
D000818:Animals; D015232:Dinoprostone / Q000502:physiology; D011464:Epoprostenol / Q000502:physiology; D006333:Heart Failure / Q000503:physiopathology*; D006801:Humans; D007668:Kidney / Q000503:physiopathology*; D011453:Prostaglandins / Q000502:physiology* / Q000627:therapeutic use; D014664:Vasodilation; D014665:Vasodilator Agents / Q000494:pharmacology
D011453:Prostaglandins; D014665:Vasodilator Agents; D011464:Epoprostenol; D015232:Dinoprostone