Usberti M, Gargiulo A, Comberti E, Campisi S, Poiesi C, Brognoli M, Doregatti C, Rondina M, Zaneboni A, Ghielmi S
Ospedale di Leno, Istituto di Chimica, Università di Brescia, Italy.
Am J Nephrol. 1989;9(4):285-90. doi: 10.1159/000167982.
To verify if exogenous prostaglandin E2 (PGE2) is able to release antidiuretic hormone (ADH) and if endogenous angiotensin II plays a role in this eventual PGE2-induced stimulation of vasopressin, increasing doses of PGE2 were infused in 6 normal volunteers before (PGE2 study) and after the administration of 100 mg of captopril (captopril study). PGE2, even at an infusion rate of 40 and 60 ng/kg/min, did not modify blood pressure when it was infused alone; a significant fall of blood pressure was observed, in contrast, in the captopril study. PGE2 alone doubled the plasma levels of ADH. One hour after the subjects had been pre-treated with captopril, plasma levels of ADH fell by about 38%, then they increased by about 60% during the infusion of PGE2. These results suggest that in normal man endogenous angiotensin II is an important non-osmotic regulator of plasma ADH and that exogenous PGE2 can stimulate maximally the release of ADH only when the renin-angiotensin system is not impaired.
