The effect of streptozotocin-induced diabetes on PGI₂ synthesis by the rat bladder

The effect of streptozotocin-induced diabetes mellitus on prostacyclin (PGI₂) production by the urinary bladder in rats was investigated. Acute ketotic (two days duration) and non-ketonuric (seven days duration) diabetes had no effect on PGI₂ production by the aorta or the bladder. 'Chronic' untreated non-ketonuric (62 days duration) diabetes had a marked inhibitory effect on aortic PGI₂ secretion which was not observed when rats were treated with insulin. Urinary bladders from animals with 'chronic' untreated non-ketonuric diabetes were larger and heavier, and their walls were hypertrophic. The bladders from these latter animals produced more total PGI₂, as well as more PGI₂ per unit weight. Enhanced PGI₂ production by bladders from animals with untreated non-ketonuric diabetes indicates that: 1) severity of the metabolic disturbance due to diabetes mellitus (ketosis) is not as important as the duration of diabetes as far as the induction of changes in PGI₂ production is concerned; 2) distension and hypertrophy of the bladder and hyperosmolar urine are probably more potent stimulators of PGI₂ production than diabetes is an inhibitor; 3) diabetes mellitus may have a variable effect on PGI₂ secretion patterns in different tissues; 4) urinary excretion of PGI₂ or its stable metabolite, 6-oxo-PGF(1α) may not exclusively reflect PGI₂ production by systemic vasculature and/or the kidneys; and 5) good control of diabetes prevents the bladder wall and PGI₂ synthesis changes.