ABSTRACT
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.
Subject(s)
Alprostadil/pharmacology , Vasopressins/blood , Adult , Aldosterone/blood , Alprostadil/blood , Blood Pressure/drug effects , Captopril/pharmacology , Catecholamines/urine , Drug Therapy, Combination , Humans , Kidney Function Tests , Male , Radioimmunoassay , Renin/bloodSubject(s)
Fluprednisolone/adverse effects , Hyperaldosteronism/chemically induced , Administration, Topical , Aged , Humans , Isomerism , MaleSubject(s)
Brucellosis/complications , Glomerulonephritis/complications , Acute Disease , Adult , Humans , MaleABSTRACT
Plasma acetate (PA) kinetics was analysed in two groups of patients on regular dialysis treatment (RDT). The first group presented frequent symptomatic hypotension (SHY), the second did not experience SHY during RDT. The parameters examined showed no difference between the two groups. Seven patients of the first group were then switched to bicarbonate dialysis. SHY rate and blood pressure changes did not significantly differ between the two methods of treatment.