Cellular interactions between vasopressin and prostaglandins in the mammalian kidney.
Current experimental evidence indicates that endogenous renal medullary prostaglandins modulate the antidiuretic response to vasopressin in the mammalian kidney. The predominant effect of prostaglandins is to attenuate the antidiuretic response to vasopressin; inhibition of prostaglandin synthesis potentiates the renal effect of vasopressin. Prostaglandins likely antagonize the renal effects of vasopressin at the cellular level of hormone-dependent cyclic adenosine 3,5-monophosphate metabolism, but the exact molecular mechanism is not known. Likewise, it is not known whether such modulatory effect is due to primary prostaglandins, prostaglandin precursors or to other metabolites of arachidonic acid. Vasopressin itself could stimulate intrarenal prostaglandin synthesis; this effect may represent a negative-feedback regulatory pathway for the antidiuretic response to the hormone. Recent experimental evidence suggests that modulatory effect of prostaglandin may be a factor in pathogenesis of some types of urinary concentrating defects.
D015105:3',5'-Cyclic-AMP Phosphodiesterases / Q000378:metabolism; D000262:Adenylyl Cyclases / Q000378:metabolism; D000818:Animals; D000242:Cyclic AMP / Q000378:metabolism; D006801:Humans; D007668:Kidney / Q000502:physiology*; D007679:Kidney Medulla / Q000378:metabolism; D011453:Prostaglandins / Q000502:physiology*; D011494:Protein Kinases / Q000378:metabolism; D014667:Vasopressins / Q000502:physiology*
D011453:Prostaglandins; D014667:Vasopressins; D000242:Cyclic AMP; D011494:Protein Kinases; D015105:3',5'-Cyclic-AMP Phosphodiesterases; D000262:Adenylyl Cyclases