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Diuretics have a number of well known adverse effects such as hyperglycaemia (or reduced carbohydrate tolerance), hyperlipidemia, hyperuricemia and hypokaliemia (1,2,3). The latter seems to mediate, at least in part, the negative effects on carbohydrate methabolism through a reduction of insulin release (4). The aim of our study has been to compare the antihypertensive and metabolic effects of a thiazide diuretic alone, thiobutizide, versus a combination of thiobutizide plus a potassium sparing agent, potassium canrenoate.

Renal prostaglandins are known to mediate the effects of loop diuretics (1,2). Muzolimine is a loop diuretic with a duration of action longer than furosemide. This feature makes this drug suitable for chronic antihypertensive therapy. The nonsteroidal antiinflammatory drugs block prostaglandin synthesis and their use may blunt the efficacy of many antihypertensive drugs (3). Indomethacin inhibits renal and systemic prostaglandins and has been also reported to interfere with the diuretic and natriuretic effects of muzolimine in man and rats (1,4). On the other hand, su-lindac, another nonsteroidal antiinflammatory drug, is known to inhibit systemic but not renal prostaglandin synthesis (3,5). The aim of this study has been therefore to verify if the antihypertensive, diuretic and humoral effects of muzolimine in man are mediated by renal prostaglandins by comparing the effects of muzolimne alone or in association with either sulindac or indomethacin.