Key result
Spironolactone markedly decreases 24-hour urinary PGE2 excretion in hypertensive rats without affecting kinin levels.
Why the study?
The effects of spironolactone on urinary prostaglandin E2 and kinin excretions in spontaneously hypertensive rats were not well characterized.
Does spironolactone reduce urinary prostaglandin E2 and kinin excretions in spontaneously hypertensive rats?
Does spironolactone reduce urinary prostaglandin E2 and kinin excretions in spontaneously hypertensive rats?
Spironolactone suppresses urinary PGE2 excretion in spontaneously hypertensive rats through a direct action rather than mediated by kinin production.
Answers are grounded in this paper and cite their sources.
Spironolactone effects in hypertensive rat models warrant no clinical changes; leaves open mechanistic and translational research.
Spironolactone was administered to spontaneously hypertensive rats (SHRs) in order to examine the urinary excretions of prostaglandin E2 (PGE2) and kinin. Thirteen SHRs were divided into 2 groups, and 0.1 ml of sesame oil was administered to one of 2 groups (spironolactone-untreated group) (n = 6) and 20 mg of spironolactone in 0.1 ml of sesame oil was administered to the other group (spironolactone-treated group) (n = 7) by the subcutaneous route for 10 days in succession, followed by the determination of body weight, blood pressure, urine volume, excretion levels of Na, K, kinin and PGE2 in 24-hour urine. Blood samples were drawn after these animals were killed by decapitation for determining plasma renin activity (PRA). In consequence, decreased blood pressure and increased urinary Na excretion were observed in the spironolactone-treated group. On the other hand, PGE2 excretion level in 24-hour urine markedly decreased immediately after administration of spironolactone (p less than 0.05) and was maintained at lower levels up to the end of experiment. However, 24-hour urinary kinin levels showed similar changes in the spironolactone-treated group and the untreated group with no significant difference between the two groups. These results indicate that spironolactone has a suppressive effect on urinary PGE2 excretion, the activity of which is not mediated by kinin production in the kidneys but produced by a direct action of spironolactone itself.
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HONDA et al. (1988) studied Hypertension (Spontaneously Hypertensive Rats) (n=13). Spironolactone vs. Sesame oil (vehicle control) was evaluated on 24-hour urinary prostaglandin E2 (PGE2) excretion (p=<0.05). Spironolactone administration in spontaneously hypertensive rats markedly decreased 24-hour urinary prostaglandin E2 excretion without affecting urinary kinin levels.
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