[Humoral and hemodynamic (systemic and renal) effects of ketanserin in patients with essential hypertension: what is the role of prostaglandins?].

We have studied the hemodynamic and humoral effects of ketanserin, an S2 antagonist, and whether PG synthesis blockade, induced by indomethacin, might modify its effects. Eight patients with uncomplicated essential hypertension were submitted to a treatment for three days with indomethacin (50 mg/b.i.d.) and for 3 days with placebo. At the end of each period, saline and ketanserin (10 mg i.v.) were given. The effects of placebo and of ketanserin were assessed for one hour by measuring the following parameters: blood pressure (BP), heart rate (HR), renal plasma flow (RPF), glomerular filtration rate (GFR), renal vascular resistance (RVR), PRA, aldosterone, noradrenaline (NA) serum and urinary thromboxane, urinary 6-keto-PGF1 alpha. Under placebo and as compared in saline, ketanserin significantly reduced BP aldosterone and RVR and increased HR, GFR, PRA, NA, serum and urinary thromboxane and urinary 6-keto-PGF1 alpha without modifying RPF. Pretreatment with indomethacin which significantly reduced serum thromboxane and urinary thromboxane and 6-keto-PGF 1 alpha prevented the renin stimulating effect and the increase in GFR induced by ketanserin without changing the other actions of this drug. Taken together, these findings indicate that PG do not play a relevant role in the antihypertensive effect of ketanserin, but mediate the GFR increase induced by this drug.