Effects of prostaglandins inhibition on changes in active and inactive renin induced by antihypertensive drugs

• Published in: Clinical and experimental hypertension. Part A, Theory and practice Vol. 4; no. 11-12; p. 2435
• Main Authors: Salvetti, A, Pedrinelli, R, Sassano, P, Arzilli, F, Turini, F
• Format: Journal Article
• Language: English
• Published: United States 1982
• Subjects: Adult; Atenolol - therapeutic use; Bumetanide - therapeutic use; Captopril - therapeutic use; Cold Temperature; Diuretics - therapeutic use; Enzyme Precursors - blood; Female; Glycolates - therapeutic use; Humans; Hypertension - drug therapy; Hypertension - enzymology; Hypertension, Renovascular - drug therapy; Hypertension, Renovascular - enzymology; Indomethacin - therapeutic use; Male; Middle Aged; Placebos; Proline - analogs & derivatives; Propanolamines - therapeutic use; Prostaglandins - physiology; Renin - blood; Ticrynafen - therapeutic use
• DOI: 10.3109/10641968209062401
• ISSN: 0730-0077

The behaviour of active (AR) and inactive (IR) renin was studied in 48 hypertensive patients (37 with uncomplicated essential hypertension and 11 with reno-vascular hypertension) treated with indomethacin alone or with AR stimulating (bumetanide, tienilic acid, captopril) and inhibiting (atenolol) drugs before and after indomethacin addition. In 10 pts indomethacin (50mg q.i.d./3 days) reduced (p less than 0.05) AR and to a lesser extent IR. In 6 pts bumetanide (1 mg) increased (p less than 0.05) only AR and this effect was abolished by indomethacin. In 6 pts tienilic acid (250 mg) increased (p less than 0.05) only AR and this action was unchanged by indomethacin. In 11 renovascular pts captopril (100mg) increased AR (p less than 0.01) and lesser IR and both these effects were uninfluenced by indomethacin. In 11 essential hypertensive pts captopril (25mg b.i.d./3 days) increased only AR (p less than 0.02), but after 1 year both AR and IR were increased (p less than 0.05) and these effects were abolished by indomethacin. In all the above reported protocols we did never find any inverse correlation between either AR and IR values or their induced changes. These data suggest that prostaglandins stimulate, even if not to a similar extent, both AR and IR and that drugs, which stimulate renin either through or independently of PGs, did not cause any apparent interconversion of plasma IR into AR. In 6 pts atenolol (100 mg daily/6 days) reduced AR (p less than 0.05) and tended to increase IR. Indomethacin addition further decreased AR and reduced IR (both p less than 0.05 vs atenolol alone): however the proportion (% of total) of IR was still reduced. These findings suggest that beta 1-adrenoreceptors blockade exerts a divergent effect on active and inactive renin and that this action is not influenced by PGs synthesis inhibition.